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1
Porowski, Dawid, Agnieszka Wirkowska, Ewa Hryniewiecka, Janusz Wyzgał, Marek Pacholczyk, and Leszek Pączek. "Liver Failure Impairs the Intrahepatic Elimination of Interleukin-6, Tumor Necrosis Factor-Alpha, Hepatocyte Growth Factor, and Transforming Growth Factor-Beta." BioMed Research International 2015 (2015): 1–7. http://dx.doi.org/10.1155/2015/934065.
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The strategic location of the liver and its metabolic activity make it a key organ regulating homeostasis. Our purpose was to examine its participation in removal of cytokines: interleukin-6 (Il-6), tumor necrosis factor-alpha (TNF-α), hepatocyte growth factor (HGF), and transforming growth factor-beta (TGF-β) from the portal circulation in human. 20 liver donors and 20 patients with end-stage liver failure were included in the study. Their blood was collected during liver transplantation from the portal, hepatic, and peripheral vein, and the hepatic artery and cytokines’ concentrations were determined. Using the results the mathematical model of cytokine elimination by the liver was developed. In donors significantly lower levels of IL-6, TNF-α, HGF, and TGF-βwere detected in portal blood compared to hepatic vein. In patients with cirrhosis there were no significant differences of IL-6, TNF-α, and TGF-βlevels between portal and hepatic veins. Significantly higher level of HGF in hepatic compared to portal vein was observed. In healthy liver elimination of the cytokines prevailed over their synthesis, as reflected by the positive values of the elimination ratios. In the cirrhotic liver elimination ratios of Il-6, HGF, and TGF-βwere negative indicating the prevalence of intrahepatic synthesis of cytokines over their removal.
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Pfeilschifter, J., W. Pignat, J. Leighton, F. Märki, K. Vosbeck, and S. Alkan. "Transforming growth factor β2 differentially modulates interleukin-1 β- and tumour-necrosis-factor-α-stimulated phospholipase A2 and prostaglandin E2 synthesis in rat renal mesangial cells." Biochemical Journal 270, no. 1 (August 15, 1990): 269–71. http://dx.doi.org/10.1042/bj2700269.
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Treatment of rat glomerular mesangial cells with transforming growth factor beta 2 (TGF beta 2) stimulates prostaglandin E2 (PGE2) synthesis. Actinomycin D, cycloheximide and diclofenac attenuate the TGF beta 2-induced PGE2 formation. As shown previously, two proinflammatory cytokines, interleukin 1 beta (IL-1 beta) and tumour necrosis factor alpha (TNF alpha), are potent stimuli for PGE2 and phospholipase A2 secretion from mesangial cells. We report here that, whereas TGF beta 2 potentiates the IL-1 β- and TNF alpha-evoked PGE2 production, it strongly inhibits the phospholipase A2 secretion induced by both cytokines. In addition, the inhibitory effect of TGF beta 2 on phospholipase A2 secretion is not due to the augmented PGE2 formation.
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Faber, Milosz, Michael Bette, Mirjam A. R. Preuss, Rojjanaporn Pulmanausahakul, Jennifer Rehnelt, Matthias J. Schnell, Bernhard Dietzschold, and Eberhard Weihe. "Overexpression of Tumor Necrosis Factor Alpha by a Recombinant Rabies Virus Attenuates Replication in Neurons and Prevents Lethal Infection in Mice." Journal of Virology 79, no. 24 (December 15, 2005): 15405–16. http://dx.doi.org/10.1128/jvi.79.24.15405-15416.2005.
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ABSTRACT The effect of tumor necrosis factor alpha (TNF-α) on rabies virus (RV) infection of the mouse central nervous system (CNS) was studied, using recombinant RV engineered to express either soluble TNF-α [SPBN-TNF-α(+)] or insoluble membrane-bound TNF-α [SPBN-TNF-α(MEM)]. Growth curves derived from infections of mouse neuroblastoma NA cells revealed significantly less spread and production of SPBN-TNF-α(+) than of SPBN-TNF-α(MEM) or SPBN-TNF-α(−), which carries an inactivated TNF-α gene. The expression of soluble or membrane-bound TNF-α was not associated with increased cell death or induction of alpha/beta interferons. Brains of mice infected intranasally with SPBN-TNF-α(+) showed significantly less virus spread than did mouse brains after SPBN-TNF-α(−) infection, and none of the SPBN-TNF-α(+)-infected mice succumbed to RV infection, whereas 80% of SPBN-TNF-α(−)-infected mice died. Reduced virus spread in SPBN-TNF-α(+)-infected mouse brains was paralleled by enhanced CNS inflammation, including T-cell infiltration and microglial activation. These data suggest that TNF-α exerts its protective activity in the brain directly through an as yet unknown antiviral mechanism and indirectly through the induction of inflammatory processes in the CNS.
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Bachmann, Anastasia, Brigitte Hanke, Rainer Zawatzky, Ubaldo Soto, Jan van Riggelen, Harald zur Hausen, and Frank Rösl. "Disturbance of Tumor Necrosis Factor Alpha-Mediated Beta Interferon Signaling in Cervical Carcinoma Cells." Journal of Virology 76, no. 1 (January 1, 2002): 280–91. http://dx.doi.org/10.1128/jvi.76.1.280-291.2002.
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ABSTRACT In the present study we show that malignant human papillomavirus (HPV)-positive cells lost their ability to synthesize endogenous beta interferon (IFN-β) upon tumor necrosis factor alpha (TNF-α) treatment. IFN-β transcription, however, was reinducible in nonmalignant HPV-positive cells, which was confirmed in functional protection assays against encephalomyocarditis virus or vesicular stomatitis virus infections. Addition of neutralizing antibodies against IFN-β blocked the antiviral effect, excluding the possibility that other IFN types were involved. Conversely, both malignant and immortalized cells could be protected against viral cytolysis when either IFN-β, IFN-α, or IFN-γ was added exogenously. This indicates that only the cross talk between TNF-α and the IFN-β pathways, and not IFN-α/β and IFN-γ signaling in general, is perturbed in cervical carcinoma cells. Notably, full virus protection was restricted exclusively to nonmalignant cells, indicating that the antiviral effect correlates with the growth-inhibitory and virus-suppressive properties of TNF-α. The IFN-regulatory factors IRF-1 and p48 (ISGF3γ) emerged as key regulatory molecules in the differential IFN-β response, since their transcription was either absent or only inefficiently enhanced in tumorigenic cells upon treatment with TNF-α. Inducibility of both genes, however, became reestablished in cervical carcinoma cells, which were complemented to nontumorigenicity after somatic cell hybridization. Complementation was paralleled by the entire reconstitution of cytokine-mediated IFN-β expression and the ability of TNF-α to exert an antiviral state. In contrast, under conditions where tumor suppression was not accomplished upon somatic cell hybridization, neither expression of IRF-1, p48, and IFN-β nor antiviral activity could be restored.
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Fan, Huizhen, Chunyan Jiang, Baoyuan Zhong, Jianwen Sheng, Ting Chen, Qingqing Chen, Jingtao Li, and Hongchuan Zhao. "Matrine Ameliorates Colorectal Cancer in Rats via Inhibition of HMGB1 Signaling and Downregulation of IL-6, TNF-α, and HMGB1." Journal of Immunology Research 2018 (2018): 1–8. http://dx.doi.org/10.1155/2018/5408324.
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Matrine may be protective against colorectal cancer (CRC), but how it may work is unclear. Thus, we explored the underlying mechanisms of matrine in CRC. Matrine-related proteins and CRC-related genes and therapeutic targets of matrine in CRC were predicted using a network pharmacology approach. Five targets, including interleukin 6 (IL-6), the 26S proteasome, tumor necrosis factor alpha (TNF-α), transforming growth factor beta 1 (TGF-β1) and p53, and corresponding high-mobility group box 1 (HMGB1) signaling and T helper cell differentiation were thought to be associated with matrine’s mechanism. Expression of predicted serum targets were verified in a 1,2-dimethylhydrazine dihydrochloride-induced CRC model rats that were treated with matrine (ip) for 18 weeks. Data show that matrine suppressed CRC growth and decreased previously elevated expression of IL-6, TNF-α, p53, and HMGB1. Matrine may have had a therapeutic effect on CRC via inhibition of HMGB1 signaling, and this occurred through downregulation of IL-6, TNF-α, and HMGB1.
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Myskiw, Chad, Janilyn Arsenio, Rebekah van Bruggen, Yvon Deschambault, and Jingxin Cao. "Vaccinia Virus E3 Suppresses Expression of Diverse Cytokines through Inhibition of the PKR, NF-κB, and IRF3 Pathways." Journal of Virology 83, no. 13 (April 15, 2009): 6757–68. http://dx.doi.org/10.1128/jvi.02570-08.
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ABSTRACT The vaccinia virus double-stranded RNA binding protein E3 has been demonstrated to inhibit the expression of cytokines, including beta interferon (IFN-β) and tumor necrosis factor alpha (TNF-α). However, few details regarding the molecular mechanisms of this inhibition have been described. Using real-time PCR arrays, we found that E3 suppressed the induction of a diverse array of cytokines representing members of the IFN, interleukin (IL), TNF, and transforming growth factor cytokine families. We discovered that the factor(s) responsible for the induction of IL-6, TNF-α, and inhibin beta A (INHBA) was associated with the early and late phases of virus infection. In contrast, the factor(s) which regulates IFN-β induction was associated with the late phase of replication. We have found that expression of these cytokines can be induced by transfection of cells with RNA isolated from vaccinia virus-infected cells. Moreover, we provide evidence that E3 antagonizes both PKR-dependent and PKR-independent pathways to regulate cytokine expression. PKR-dependent activation of p38 and NF-κB was required for vaccinia virus-induced INHBA expression, whereas induction of TNF-α required only PKR-dependent NF-κB activation. In contrast, induction of IL-6 and IFN-β was largely PKR independent. IL-6 induction is regulated by NF-κB, while IFN-β induction is mediated by IFN-β promoter stimulator 1 and IFN regulatory factor 3/NF-κB. Collectively, these results indicate that E3 suppresses distinct but interlinked host signaling pathways to inhibit the expression of a diverse array of cytokines.
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Fritzgerald, Richard, Cecilia Lunardhi, Ruslan Effendy, and Tamara Yuanita. "EKSPRESI Tumor Necrosis Factor alpha (TNF-α) DAN Transforming growth factors beta (TGF-β) PADA PERIODONTITIS APIKALIS KRONIS AKIBAT INDUKSI Enterococcus faecalis PADA TIKUS WISTAR." Conservative Dentistry Journal 7, no. 2 (December 5, 2019): 66. http://dx.doi.org/10.20473/cdj.v7i2.2017.66-73.
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Background. Root canal treatment is a main role in decreasing infection from root canal and pulp. The main cause of periapical damage mostly are bacteries. E.faecalis is a bactery that is found as an etiology of endodontic treatment failure. Cell wall of this bacteria is containing Lipoteichoic acid (LTA). LTA can penetrate into the periradicular tissue, act as endotoxin in host and cause periradicular inflammation then lead to bone destruction. LTA stimulates immunology reaction that produce Tumor Necrosis Factor alpha (TNF-α) and Transforming growth factors beta (TGF-ß). TNF-α is a main mediator and also have an important role in inflamation response otherwise TGF-ß is working as a multifunction regulator of cell growth and differentiation during reforming and remodelling. Purpose. The aim of this study is to know about the expression of TNF-α and TGF-ß during the periapical tissue damage due to induction of E.faecalis. Method. This study used laboratory experimental with the post test only control group design. A total of 30 male rats were randomly divided into 3 main groups, Group A (control negative) : normal tooth. Group B (control positive) : every tooth was induced only by sterile BHI-b. Group C (treated group) : every tooth was induced by 10 μl BHI-b E.faecalis ATCC212(106 CFU). The animals were sacrificed 21 days later and prepared for histological examination of tissue damage, then we did the immunohistochemistry followed by calculation on the light microscope. Result. The analysis revealed that the expression of TNF-α at treated group are higher than negative control and positive control but the expression of TGF-ß at treated group are higher than the negative control group but lower than positive control. Conclusion. From this study we know that the expression of TNF-α and TGF-ß are changing during the periapical tissue damage that induced by E.faecalis.
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Peresi, Eliana, Sônia Maria Usó Ruiz Silva, Sueli Aparecida Calvi, and Jussara Marcondes-Machado. "Citocinas e proteínas de fase aguda do soro como marcadores de regressão da resposta inflamatória ao tratamento da tuberculose pulmonar." Jornal Brasileiro de Pneumologia 34, no. 11 (November 2008): 942–49. http://dx.doi.org/10.1590/s1806-37132008001100009.
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OBJETIVO: Analisar o padrão de citocinas pró- e antiinflamatórias e da resposta de fase aguda (RFA) como marcadores de resposta ao tratamento da tuberculose pulmonar. MÉTODOS: Determinação dos níveis de interferon-gama (IFN-γ), tumor necrosis factor-alpha (TNF-α, fator de necrose tumoral-alfa), interleucina-10 (IL-10) e transforming growth factor-beta (TGF-β, fator transformador de crescimento-beta), pelo método ELISA, em sobrenadante de cultura de células mononucleares do sangue periférico e monócitos, assim como dos níveis de proteínas totais, albumina, globulinas, alfa-1-glicoproteína ácida (AGA), proteína C reativa (PCR) e velocidade de hemossedimentação (VHS) em 28 doentes com tuberculose pulmonar, em três tempos: antes (T0), aos três meses (T3) e aos seis meses (T6) de tratamento, em relação aos controles saudáveis, em um único tempo. RESULTADOS: Os pacientes apresentaram valores maiores de citocinas e RFA que os controles em T0, com diminuição em T3 e diminuição (TNF-α, IL-10, TGF-β, AGA e VHS) ou normalização (IFN-γ e PCR) em T6. CONCLUSÕES: PCR, AGA e VHS são possíveis marcadores para auxiliar no diagnóstico de tuberculose pulmonar e na indicação de tratamento de indivíduos com baciloscopia negativa; PCR (T0 > T3 > T6 = referência) pode também ser marcador de resposta ao tratamento. Antes do tratamento, o perfil Th0 (IFN-γ, IL-10, TNF-α e TGF-β), indutor de e protetor contra inflamação, prevaleceu nos pacientes; em T6, prevaleceu o perfil Th2 (IL-10, TNF-α e TGF-β), protetor contra efeito nocivo pró-inflamatório do TNF-α ainda presente. O comportamento do IFN-γ (T0 > T3 > T6 = controle) sugere sua utilização como marcador de resposta ao tratamento.
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Hsu, Li-Han, Thomas C. Soong, Nei-Min Chu, Chung-Yu Huang, Shu-Huei Kao, and Yung-Feng Lin. "The Inflammatory Cytokine Profile of Patients with Malignant Pleural Effusion Treated with Pleurodesis." Journal of Clinical Medicine 9, no. 12 (December 11, 2020): 4010. http://dx.doi.org/10.3390/jcm9124010.
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Patients with malignant pleural effusion (MPE) who underwent successful pleurodesis survive longer than those for whom it fails. We hypothesize that the therapy-induced inflammatory responses inhibit the cancer progression, and thereby lead to a longer survival. Thirty-three consecutive patients with MPE that were eligible for bleomycin pleurodesis between September 2015 and December 2017 were recruited prospectively. Nineteen patients (57.6%) achieved fully or partially successful pleurodesis, while 14 patients either failed or survived less than 30 days after pleurodesis. Two patients without successful pleurodesis were excluded because of missing data. Interleukin (IL)-1 beta, IL-6, IL-10, transforming growth factor beta, tumor necrosis factor alpha (TNF-α), and vascular endothelial growth factor in the pleural fluid were measured before, and after 3 and 24 h of pleurodesis. Their pleurodesis outcome and survival were monitored and analyzed. Patients who underwent successful pleurodesis had a longer survival rate. Patients without successful pleurodesis had significantly higher TNF-α and IL-10 levels in their pleural fluid than in the successful patients before pleurodesis. Following pleurodesis, there was a significant increment of IL-10 in the first three hours in the successful patients. In contrast, significant increments of TNF-α and IL-10 were found in the unsuccessful patients between 3 and 24 h after pleurodesis. The ability to produce specific cytokines in the pleural space following pleurodesis may be decisive for the patient’s outcome and survival. Serial measurement of cytokines can help allocate the patients to adequate treatment strategies. Further study of the underlying mechanism may shed light on cytokine therapies as novel approaches.
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Jelodar, Gholamali, Mansour Azimzadeh, Fatemeh Radmard, and Narges Darvishhoo. "Alteration of intrapancreatic serotonin, homocysteine, TNF-α, and NGF levels as predisposing factors for diabetes following exposure to 900-MHz waves." Toxicology and Industrial Health 37, no. 8 (June 21, 2021): 496–503. http://dx.doi.org/10.1177/07482337211022634.
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Exposure to mobile phone radiation causes deleterious health effects on biological systems. The objects of this study were to investigate the effect of 900-MHz radiofrequency waves (RFW) emitted from base transceiver station antenna on intrapancreatic homocysteine (Hcy), tumor necrosis factor-α (TNF-α), and nerve growth factor (NGF) as predisposing factors involved in pancreatic beta cell damage. Thirty male rats (Sprague-Dawley, 200 ± 10 g) were randomly divided into the control (without any exposure) and exposed groups: short time (2 h/day), long time (4 h/day), and exposed to 900-MHz RFW for 30 consecutive days. On the last days of the experiment, animals were killed and pancreas tissue was dissected out for evaluation of serotonin, Hcy, TNF-α, and NGF. There was a significant decrease in the serotonin and NGF levels in the pancreatic tissue of exposed groups compared to the control group ( p < 0.05). Also, the levels of serotonin and NGF in the long-time exposure were significantly lower than the short-time exposure ( p < 0.05). However, levels of Hcy and TNF-α were significantly increased in the pancreas of exposed groups compared to the control groups ( p < 0.05). Exposure to 900-MHz RFW decreased pancreatic NGF and serotonin levels and increased the proinflammatory markers (Hcy and TNF-α), which can be a predisposing factor for type 2 diabetes.
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Ramadan, Abeer, Sara Sallam, Rasha Yousef, Mai Elsheikh, Asmaa Ali, Yasmine Elhusseny, and Sally Ishak. "Evaluation of IGF-1, TNF-α, and TGF-β Gene Expression after Oral Vitamin D Supplementation in School-Aged Children with Chronic Bronchial Asthma." Open Access Macedonian Journal of Medical Sciences 10, B (May 19, 2022): 1358–64. http://dx.doi.org/10.3889/oamjms.2022.9266.
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BACKGROUND: Airway remodeling in children with bronchial asthma is due to the effect of inflammatory mediators and growth factors on the bronchial epithelium. Vitamin D (VitD) has immunomodulatory effect in many inflammatory diseases as bronchial asthma. The ant-inflammatory and anti-fibrotic role of VitD could prevent or improve air way remodeling in asthmatic patients. AIM: The study investigated the effect of VitD supplementation on the expression of transforming growth factor-beta (TGF-β), tumor necrosis factor-alpha (TNF-α), and insulin growth factor 1(IGF-1) and to correlate them with asthma severity and level of control. METHODS: The serum level of VitD and the mRNA expression of IGF-1, TGF-β, and TNF-α were estimated in 50 patients and 20 healthy controls control subjects using quantitative PCR in real-time. Asthmatic patients with VitD deficiency received VitD supplementation for 2 months followed by remeasurement of serum VitD and the genes expression TGF-β, TNF-α, and IGF-1. RESULT: Pre-intake of VitD and serum level of VitD were lower in all patients than control subjects (p = 0.005). VitD level was directly correlated with IGF-1 mRNA expression, which was indirectly correlated with TGF-β, r = 0.5 and −0.57; p = 0.0001 and 0.002, respectively. After VitD supplementation, the expression of the TGF-β mRNA gene was the only gene that decreased significantly (p = 0.04) together with improved asthma control and spirometric parameters. CONCLUSIONS: VitD supplementation down regulated the gene expression of TGF-β and improved asthma control level, but it did not significantly affect the gene expression of TNF-α and IGF-1.
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Chilliveri, Prashant, Baluka Vanitha, and Y. Shiva Kumar. "Genetic Predisposition of TNF-α (-308), TGF-β-1 (-508) and IL-35(EBI3) Gene Polymorphisms towards Rheumatic Heart Disease in the Population of Telangana from South India." International Journal of Health Sciences and Research 12, no. 12 (December 8, 2022): 1–6. http://dx.doi.org/10.52403/ijhsr.20221201.
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Background: Rheumatic Heart Disease (RHD) is a complex disease, subject to genetic and environmental factors. Cytokines play an important role in development and pathogenesis of the rheumatic heart disease. TNF-α, TGF-β and IL-35 gene polymorphisms may affect the expression levels of cytokines which may lead to damage to the heart valves. Objective: This study was intended to explore the association of TNF-α, TGF-β and IL-35 gene polymorphisms with RHD. Materials and Methods: The present case control study consisted of 145 patients with rheumatic heart disease and 217 control subjects in the same age group. Genotyping was done for the TNF-α (-308), TGF-β-1 (-508) and IL-35(EBI3) gene polymorphisms in both case and control groups. Results: The results showed Bone differences in the distribution of genotypes in TNF-α, TGF-β and IL-35 genes RHD cases and control groups. However, the statistical analysis of the data showed the differences in the genotypes between TNF alpha (-308 G>A), TGF-β-1 (C-508T) and IL-35 EBI3G/C genes RHD case and control subjects were not found to be statistically significant. Conclusion: In conclusion our study could not find any significant association between TNF-α (-308), TGF-β-1 (-508) and IL-35(EBI3) gene polymorphisms and RHD. Key words: Rheumatic Heart Disease, Cytokines, Tumour Necrosis Factor alpha, Transforming growth factor beta 1, Interleukin, Single Nucleotide Polymorphism.
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Pengzong, Zhang, Li Yuanmin, Xiong Xiaoming, Deng Shang, Xiong Wei, Lang Zhigang, Du Dongzhou, et al. "Wound Healing Potential of the Standardized Extract of Boswellia serrata on Experimental Diabetic Foot Ulcer via Inhibition of Inflammatory, Angiogenetic and Apoptotic Markers." Planta Medica 85, no. 08 (March 25, 2019): 657–69. http://dx.doi.org/10.1055/a-0881-3000.
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AbstractThe aim of the present study was to evaluate the wound healing potential and possible mechanism of action of the standardized extract of Boswellia serrata against the experimental model of diabetic foot ulcer. α-Boswellic acid was isolated from the standardized extract of B. serrata and characterized (HPLC, 1H-NMR, 13C-NMR, ESI-MS). Diabetes was induced in Sprague-Dawley rats by streptozotocin (55 mg/kg, i. p.), and wounds were created on the dorsal surface of the hind paw. B. serrata (100, 200, and 400 mg/kg, p. o.) was administered to the rats for 16 days. The HPLC analysis showed a single peak with a retention time of 12.51 min. The compound was identified with ESI-MS [M + Na]+ = 455.37 as α-boswellic acid. Treatment with B. serrata (200 and 400 mg/kg) significantly increased the rate of wound contraction via modulation of oxido-nitrosative stress and elevated the hydroxyproline level at the wound area. reverse transcription-PCR analysis revealed that streptozotocin-induced increases in TNF-α, interleukin-1β, interleukin-6, nuclear factor-kappa-light-chain-enhancer of activated B cells, and Bcl-2-associated X protein, and decreases in angiopoietin-1, Tie2, transforming growth factor beta 1, vascular endothelial growth factor, and collagen-1 mRNA expression were significantly inhibited by B. serrata. It also significantly reduced wound cellular necrosis as evaluated by flow cytometry using propidium iodide fluorescence intensity. Streptozotocin-induced histopathological alterations were also significantly ameliorated by B. serrata. In conclusion, standardized extracts of B. serrata exert its wound healing potential via orchestrating mechanisms, which include the inhibition of oxido-inflammatory markers (oxido-nitrosative stress, TNF-α, interleukins, and nuclear factor-kappa-light-chain-enhancer of activated B cells), increased collagen synthesis (hydroxyproline and collagen-1) and angiogenesis (Ang-1/Tie2), promoting growth factors (transforming growth factor beta 1 and vascular endothelial growth factor), and inhibition of apoptosis (Bcl-2-associated X protein) to accelerate wound healing in experimental delayed diabetic foot ulcer.
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Thornburg, Natalie J., Bryan Shepherd, and James E. Crowe. "Transforming Growth Factor Beta Is a Major Regulator of Human Neonatal Immune Responses following Respiratory Syncytial Virus Infection." Journal of Virology 84, no. 24 (October 6, 2010): 12895–902. http://dx.doi.org/10.1128/jvi.01273-10.
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ABSTRACT Respiratory syncytial virus (RSV) is a major cause of morbidity and mortality. Previous studies have suggested that T-cell responses may contribute to RSV immunopathology, which could be driven by dendritic cells (DCs). DCs are productively infected by RSV, and during RSV infections, there is an increase of DCs in the lungs with a decrease in the blood. Pediatric populations are particularly susceptible to severe RSV infections; however, DC responses to RSV from pediatric populations have not been examined. In this study, primary isolated DCs from cord blood and adult peripheral blood were compared after RSV infection. Transcriptional profiling and biological network analysis identified transforming growth factor beta (TGF-β) and associated signaling molecules as differentially regulated in the two age groups. TGF-β1 was decreased in RSV-infected adult-blood DCs but increased in RSV-infected cord blood DCs. Coculture of adult RSV-infected DCs with autologous T cells induced secretion of gamma interferon (IFN-γ), interleukin 12p70 (IL-12p70), IL-2, and tumor necrosis factor alpha (TNF-α). Conversely, coculture of cord RSV-infected DCs and autologous T cells induced secretion of IL-4, IL-6, IL-1β, and IL-17. Addition of purified TGF-β1 to adult DC-T-cell cocultures reduced secretion of IFN-γ, IL-12p70, IL-2, and TNF-α, while addition of a TGF-β chemical inhibitor to cord DC-T-cell cocultures increased secretion of IL-12p70. These data suggest that TGF-β acts as a major regulator of RSV DC-T-cell responses, which could contribute to immunopathology during infancy.
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Pasquetto, Valérie, Stefan F. Wieland, Susan L. Uprichard, Marco Tripodi, and Francis V. Chisari. "Cytokine-Sensitive Replication of Hepatitis B Virus in Immortalized Mouse Hepatocyte Cultures." Journal of Virology 76, no. 11 (June 1, 2002): 5646–53. http://dx.doi.org/10.1128/jvi.76.11.5646-5653.2002.
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ABSTRACT We have previously shown that alpha/beta interferon (IFN-α/β) and gamma interferon (IFN-γ) inhibit hepatitis B virus (HBV) replication by eliminating pregenomic RNA containing viral capsids from the hepatocyte. We have also shown that HBV-specific cytotoxic T lymphocytes that induce IFN-γ and tumor necrosis factor alpha (TNF-α) in the liver can inhibit HBV gene expression by destabilizing preformed viral mRNA. In order to further study the antiviral activity of IFN-α/β, IFN-γ, and TNF-α at the molecular level, we sought to reproduce these observations in an in vitro system. Accordingly, hepatocytes were derived from the livers of HBV-transgenic mice that also expressed the constitutively active cytoplasmic domain of the human hepatocyte growth factor receptor (c-Met). Here, we show that the resultant well-differentiated, continuous hepatocyte cell lines (HBV-Met) replicate HBV and that viral replication in these cells is efficiently controlled by IFN-α/β or IFN-γ, which eliminate pregenomic RNA-containing capsids from the cells as they do in the liver. Furthermore, we demonstrate that IFN-γ, but not IFN-α/β, is capable of inhibiting HBV gene expression in this system, especially when it acts synergistically with TNF-α. These cells should facilitate the analysis of the intracellular signaling pathways and effector mechanisms responsible for these antiviral effects.
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Chen, Chin-Chuan, Hung-Yuan Li, Yann-Lii Leu, Yu-Ju Chen, Chia-Jen Wang, and Shu-Huei Wang. "Corylin Inhibits Vascular Cell Inflammation, Proliferation and Migration and Reduces Atherosclerosis in ApoE-Deficient Mice." Antioxidants 9, no. 4 (March 25, 2020): 275. http://dx.doi.org/10.3390/antiox9040275.
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Atherosclerosis is a complex disease that includes several events, including reactive oxygen species (ROS) stress, inflammation, endothelial dysfunction, lipid deposition, and vascular smooth muscle cell (VSMC) proliferation and migration, which result in atherosclerotic plaque formation. Corylin, a flavonoid compound, is known to exhibit antioxidative, anti-inflammatory and antiproliferative effects. However, it remains unknown whether corylin could modulate atherogenesis. Here, we identified the anti-inflammatory effect of corylin in tumor necrosis factor-α (TNF-α)-induced vascular cells. In human umbilical vein endothelial cells (HUVECs), corylin suppressed TNF-α-induced monocyte adhesion to the HUVECs and transmigration by downregulating the ROS/JNK/nuclear factor-kappa beta (NF-κB) p65 pathway. In VSMCs, corylin inhibited TNF-α-induced monocyte adhesion by suppressing ROS production, mitogen-activated protein kinase (MAPK) phosphorylation and NF-κB p65 translocation. In platelet-derived growth factor-BB (PDGF-BB)-induced VSMCs, corylin inhibited PDGF-BB-induced VSMC proliferation and migration through regulating the mammalian target of rapamycin (mTOR)/dynamin-1-like protein 1 (Drp1) signaling cascade. In addition, corylin treatment not only attenuated atherosclerotic lesions, ROS production, vascular cell adhesion protein-1 (VCAM-1) expression, monocyte adhesion and VSMC proliferation in apolipoprotein E (ApoE)-deficient mice but also inhibited neointimal hyperplasia in endothelial-denuded mice. Thus, corylin may be a potential prevention and treatment for atherosclerosis.
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H. Bayoumi, Ahmed, Ahmed El Zainy, Amul M. Badr, Dina Fawzy, and Amal A. Elshimy. "Assessment of Therapeutic Efficacy of Mesenchymal Stem Cells in Doxorubicin- Induced Skeletal Myopathy: A histological and Immunological Experimental Study." Egyptian Journal of Medical Microbiology EJMM29, no. 4 (October 1, 2020): 35–44. http://dx.doi.org/10.51429/ejmm29405.
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Background: Doxorubicin is an effective chemotherapeutic drug that commonly induce pathological alteration in skeletal muscles. Bone- marrow mesenchymal stem cells (BMMSCs) offer a therapeutic potential for tissue repair and regeneration. Tumour necrosis factor-alpha (TNF-α) and Interleukin-1 beta (IL-1β) display worthy biomarkers for tissue damage and repair. Objectives: The aim of the current study was to evaluate the therapeutic effect of BMMSCs on doxorubicin - induced skeletal myopathy in experimental animals, through histological studies, antioxidant activity and investigation of TNF-α, IL-1β as diagnostic parameters for muscle damage and regeneration. Methodology: 40 adult albino-rats were divided into 4 equal groups; Group-I (control group) injected with phosphate-buffered saline (PBS), Group-II: doxorubicin- induced myopathy model group; received no treatment, Group-III: doxorubicin- induced myopathy model left for spontaneous muscle recovery, and Group-IV: doxorubicin- induced myopathy treated with systemic BMMSCs. The skeletal muscle regeneration evaluated through histological and antioxidant activity studies and investigation of TNF-α, IL-1β and vascular endothelial growth factor (VEGF) levels. Results: Photomicrographic studies of the muscle fibers showed a more evident regeneration in MSCs treated groups (IV) when compared with the other groups received no treatment. A significant reduced levels of TNF-α, IL-1β, and increased both VEGF and antioxidant activity were demonstrated in group IV when compared with the other groups received no treatment. Conclusion: MSCs is a promising therapy for doxorubicin-induced skeletal myopathy. TNF-α, and IL-1β are helpful biomarkers for evaluation of SCs therapeutic efficacy.
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Chen, Wei, Prabhu Balan, and David G. Popovich. "The Effects of New Zealand Grown Ginseng Fractions on Cytokine Production from Human Monocytic THP-1 Cells." Molecules 26, no. 4 (February 22, 2021): 1158. http://dx.doi.org/10.3390/molecules26041158.
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Pro-inflammatory cytokines and anti-inflammatory cytokines are important mediators that regulate the inflammatory response in inflammation-related diseases. The aim of this study is to evaluate different New Zealand (NZ)-grown ginseng fractions on the productions of pro-inflammatory and anti-inflammatory cytokines in human monocytic THP-1 cells. Four NZ-grown ginseng fractions, including total ginseng extract (TGE), non-ginsenoside fraction extract (NGE), high-polar ginsenoside fraction extract (HPG), and less-polar ginsenoside fraction extract (LPG), were prepared and the ginsenoside compositions of extracts were analyzed by HPLC using 19 ginsenoside reference standards. The THP-1 cells were pre-treated with different concentrations of TGE, NGE, HPG, and LPG, and were then stimulated with lipopolysaccharide (LPS). The levels of pro-inflammatory cytokines, including tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), interleukin-6 (IL-6), interleukin-8 (IL-8), and anti-inflammatory cytokines, such as interleukin-10 (IL-10), and transforming growth factor beta-1 (TGF-β1), were determined by enzyme-linked immunosorbent assay (ELISA). TGE at 400 µg/mL significantly inhibited LPS-induced TNF-α and IL-6 productions. NGE did not show any effects on inflammatory secretion except inhibited IL-6 production at a high dose. Furthermore, LPG displayed a stronger effect than HPG on inhibiting pro-inflammatory cytokine (TNF-α, IL-1β, and IL-6) productions. Particularly, 100 µg/mL LPG not only significantly inhibited the production of pro-inflammatory cytokines TNF-α, IL-1β, and IL-6, but also remarkably enhanced the production of anti-inflammatory cytokine IL-10. NZ-grown ginseng exhibited anti-inflammatory effects in vitro, which is mainly attributed to ginsenoside fractions (particularly less-polar ginsenosides) rather than non-saponin fractions.
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Cunha, F. Q., and W. M. S. Cunha Tamashiro. "Tumour necrosis factor-alpha and interleukin-8 inhibit neutrophil migration in vitro and in vivo." Mediators of Inflammation 1, no. 6 (1992): 397–401. http://dx.doi.org/10.1155/s0962935192000607.
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Pretreatment of human neutrophils with recombinant tumour necrosis factor-alpha (rTNF-α) and/or interleukin-8 (rIL-8), but not with either transforming growth factor-beta, interleukin-6 or interferon-gamma, rendered these cells less responsive to FMLP, in microchemotaxis assays. This inhibitory effect was dose dependent and more powerful when neutrophils were pretreated with a mixture of both cytokines. Intravenous injection of human rIL-8 (hrIL-8) and/or murine rTNF-α (mrTNF-α) also significantly reduced in vivo neutrophil migration into peritoneal cavities of rats stimulated with carrageenan. These data suggest that the defect in neutrophil migration during septicaemia or endotoxaemia may be the result of the continuous release of IL-8 and TNF-α into the circulation. Thus, either the selective control or blockade of releasing of these cytokines as well as of its effects on neutrophils may be clinically useful in reestablishing the cell defence mechanisms.
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Abdulmawjood, Bilal, Beatriz Costa, Catarina Roma-Rodrigues, Pedro V. Baptista, and Alexandra R. Fernandes. "Genetic Biomarkers in Chronic Myeloid Leukemia: What Have We Learned So Far?" International Journal of Molecular Sciences 22, no. 22 (November 19, 2021): 12516. http://dx.doi.org/10.3390/ijms222212516.
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Chronic Myeloid Leukemia (CML) is a rare malignant proliferative disease of the hematopoietic system, whose molecular hallmark is the Philadelphia chromosome (Ph). The Ph chromosome originates an aberrant fusion gene with abnormal kinase activity, leading to the buildup of reactive oxygen species and genetic instability of relevance in disease progression. Several genetic abnormalities have been correlated with CML in the blast phase, including chromosomal aberrations and common altered genes. Some of these genes are involved in the regulation of cell apoptosis and proliferation, such as the epidermal growth factor receptor (EGFR), tumor protein p53 (TP53), or Schmidt-Ruppin A-2 proto-oncogene (SRC); cell adhesion, e.g., catenin beta 1 (CTNNB1); or genes associated to TGF-β, such as SKI like proto-oncogene (SKIL), transforming growth factor beta 1 (TGFB1) or transforming growth factor beta 2 (TGFB2); and TNF-α pathways, such as Tumor necrosis factor (TNFA) or Nuclear factor kappa B subunit 1 (NFKB1). The involvement of miRNAs in CML is also gaining momentum, where dysregulation of some critical miRNAs, such as miRNA-451 and miRNA-21, which have been associated to the molecular modulation of pathogenesis, progression of disease states, and response to therapeutics. In this review, the most relevant genomic alterations found in CML will be addressed.
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Argilés, J. M., F. J. López-Soriano, D. Wiggins, and D. H. Williamson. "Comparative effects of tumour necrosis factor-α (cachectin), interleukin-1-β and tumour growth on amino acid metabolism in the rat in vivo. Absorption and tissue uptake of α-amino[1-14C]isobutyrate." Biochemical Journal 261, no. 2 (July 15, 1989): 357–62. http://dx.doi.org/10.1042/bj2610357.
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The effects of acute administration of either tumour necrosis factor-alpha (cachectin) (TNF) or interleukin-1-beta (IL-1), or of tumour growth (Walker-256 carcinosarcoma), on blood amino acid concentrations and tissue alpha-amino[1-14C]isobutyrate (AIB) uptake in virgin and lactating rats were compared. Both monokines decreased the blood concentrations of those amino acids (serine, glycine, alanine and proline) transported via the A system. Tumour growth decreased the blood concentrations of serine, proline and histidine, whereas the concentrations of glutamine and leucine were increased. IL-1 decreased the intestinal absorption of AIB in all groups studied; TNF or tumour growth had no effect. Tissue AIB uptake was increased (1.5-2.5-fold) in liver, whereas it was decreased in heart and skeletal muscle of the three treatment groups (except skeletal muscle of the IL-1-treated rats). Lactating rats had lower hepatic uptake of AIB compared with livers of virgin rats. IL-1 increased the hepatic uptake of AIB in lactating rats, but not to the values seen in virgin rats treated with IL-1; there was no effect of the cytokine on muscle or mammary-gland uptake. In adrenalectomized rats, the stimulatory effect of IL-1 on hepatic AIB uptake was diminished, whereas that of TNF still persisted. IL-1 caused a marked decrease of AIB uptake in muscle and heart of adrenalectomized rats, which was accompanied by an increase in the blood concentrations of branched-chain amino acids. These effects did not occur with TNF. It is concluded that the effects of the cytokines on tissue amino acid metabolism may depend on a differential endocrine response involving glucagon and/or glucocorticoids.
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Xue, Hai-Yan, Ming-Wei Liu, and Guang Yang. "Resveratrol suppresses lipopolysaccharide-mediated activation of osteoclast precursor RAW 264.7 cells by increasing miR-181a-5p expression." International Journal of Immunopathology and Pharmacology 37 (February 1, 2023): 039463202311549. http://dx.doi.org/10.1177/03946320231154995.
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Resveratrol (Res) has anti-inflammation and antiosteoporosis functions. We evaluated the effect of Res on osteoclast differentiation by releasing inflammatory cytokines from osteoclast precursor RAW 264.7 cells stimulated by lipopolysaccharide (LPS). In the study, LPS (1 ng/L) was used to induce the Raw 264.7 inflammatory injury model in vitro. A total of 25 ng/mL M-CSF + 30 ng/mL RANKL or plus 1 μg/L LPS was used to induce osteoclastogenesis in the experiments. We utilized the Cell Counting Kit-8 assay to measure the relative cell survival of RAW 264.7 cells. Then, enzyme-linked immunosorbent assays were utilized to measure the abundance of inflammatory markers, such as interleukin-1 beta (IL-1β), tumor necrosis factor-alpha (TNF-α), and IL-6. Subsequently, Western blot analysis was applied to assess the abundance of phosphorylated transforming growth factor beta-activated kinase 1 (P-TAK1) protein, TNF receptor-associated factor 6 (TRAF6), nuclear factor-κB inhibitor protein (IκB), phosphorylated IκB-α (P-IκB-α), and nuclear factor κB65 (NF-κB65). mRNA expression levels of miR-181a-5p, TRAF6, specific gene calcitonin receptor (CTR), activated T nuclear factor 1 (NFATC1), cathepsin K (CTSK), and matrix metalloproteinase (MMP)-9 were determined via a real-time polymerase chain reaction. Osteoclast bone resorption function was determined. Finally, tartrate-resistant acid phosphatase (TRAP) staining was performed.The results found that Compared with the model group, the degrees of expressions of supernatant inflammatory factors TNF-α, IL-1β, and IL-6 were substantially attenuated in the Res treatment group ( p < 0.05). Furthermore, the extent of miR-181a-5p expression in the RAW 264.7 cells significantly increased, whereas P-IκB-α, P-TAK1, NF-κB65, and TRAF6 expressions significantly decreased in the Res treatment group as opposed to the model group ( p < 0.05). The CTR, NFATC1, MMP-9, CTSK, and TRAP mRNA expression levels were substantially reduced during osteoclast differentiation and bone resorption in the Res treatment group.The results suggest that Res can reduce the RAW 264.7 cell differentiation into osteoclasts and relieve LPS-stimulated osteoporosis, and the underlying mechanism may be associated with the Res-inhibited activity of the TRAF6/TAK1 pathway through the increased miR-181a-5p expression.
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Ma, Yanzhen, Shaopeng Huang, Hui Jiang, and Wenming Yang. "Mechanism of Zhinao Capsule in Treating Alzheimer’s Disease Based on Network Pharmacology Analysis and Molecular Docking Validation." Journal of Healthcare Engineering 2022 (August 18, 2022): 1–12. http://dx.doi.org/10.1155/2022/5708769.
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Objective. This study aimed to determine the active components of Zhinao capsule (ZNC) and the targets in treating Alzheimer’s disease (AD) so as to investigate and explore the mechanism of ZNC for AD. Methods. The active components and targets of ZNC were determined from the traditional Chinese medicine systems pharmacology database (TCMSP). The target genes of AD were searched for in GeneCards. Cytoscape was used to construct an herb-component-target-disease network. A protein-protein interaction (PPI) network was constructed by STRING. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed using the OmicShare. UCSF Chimera and SwissDock were used for molecular docking verification. Finally, four key target genes were validated by Western blotting. Results. In total, 55 active components, 287 targets of active components, 1197 disease genes, and 134 common genes were screened, which were significantly enriched in 3975 terms of biological processes (BP), 284 terms of cellular components (CC), 433 terms of molecular functions (MF), and 245 signaling pathways. Caspase-3 (CASP3) and beta-sitosterol, tumor necrosis factor-alpha (TNF-α) and quercetin, vascular endothelial growth factor A (VEGFA) and baicalein, and mitogen-activated protein kinase 1 (MAPK1) and quercetin showed good-to-better docking. Moreover, ZNC not only downregulated CASP3 and TNF-α protein expression but also upregulated the protein expression of VEGFA and MAPK1. Conclusions. The active components of ZNC, such as beta-sitosterol, quercetin, and baicalein may act on multiple targets like CASP3, VEGFA, MAPK1, and TNF-α to affect T cell receptor (TCR), TNF, and MAPK signaling pathway, thereby achieving the treatment of AD. This study provides a scientific basis for further exploring the potential mechanism of ZNC in the treatment of AD and a reference for its clinical application.
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Endah Kamila Mas’udah, Dwi Yuni Nur Hidayati, Sanarto Santoso, Wuri Widi Astuti, Anna Malia, and Dyah Woro Kartiko Kusumo Wardani. "The effect of red Turi leaf extract (Sesbania glandiflora L.Pers) on the reduced levels of TNF-α, IL-1β and the number of bacterial colonies on the puerperium Mus Musculus ovarian inoculated by Staphylococcus aureus." GSC Biological and Pharmaceutical Sciences 18, no. 2 (February 28, 2022): 344–49. http://dx.doi.org/10.30574/gscbps.2022.18.2.0085.
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Staphylococcus aureus is one of the bacteria that causes postpartum infection, where this bacterium releases peptidoglycans and lipoteichoic acid (LTA) that start the inflammation response, which is then responded by macrophages by releasing pro-inflammation cytokines such as Tumor Necrosis Factor-Alpha (TNF-α) and Interleukin 1-Beta (IL-1β). Red Turi leaf extract, which is known to contain saponins, flavonoids, and tannins which work by suppressing the growth of bacteria and forcing bacterial cells to undergo lysis, causing the reduction of immune system activation which results in the reduction of secretion of pro-inflammation cytokines such as TNF-α and IL-1β. This research aims to analyze the effect of red Turi leaf extract in reducing TNF-α, IL-1β, and bacterial colonies on the puerperium Mus Musculus Ovarian Inoculated by Staphylococcus aureus. Results in this study proved that red Turi leaf extract of doses of 125, 250, and 500 mg/kgBW/day was able to reduce TNF-α, IL-1β, and the number of bacterial colonies on the puerperium Mus Musculus Ovarian Inoculated by Staphylococcus aureus. The optimum doses to reduce the number of bacterial colonies were doses of 250 and 500 mg/kgBW/day. Thus, the infection caused by intravaginal inoculation Staphylococcus aureus for 24 hours on the puerperium Mus Musculus Ovary was alleviated by treatment with red Turi leaf extract by reducing TNF-α, IL-1β, and the number of bacterial colonies on the puerperium Mus Musculus Ovarian Inoculated by Staphylococcus aureus.
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Kanangat, Sivadasan, Sanjib Basu, Ina Kurbecovic, Michele Prod, John Joseph Maciejewski, Sunita Nathan, Henry C. Fung, and Elizabeth Shima Rich. "Transforming growth factor-beta gene polymorphisms and acute graft-versus-host disease." Journal of Clinical Oncology 31, no. 15_suppl (May 20, 2013): e18013-e18013. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.e18013.
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e18013 Background: Despite allele level HLA matching, graft-versus-host disease (GVHD) remains a major complication of allogeneic hematopoietic cell transplantation (HCT). Differences in minor histocompatibility antigens impact GVHD and HCT outcome via activation of donor T cells that also mediate a graft-versus-leukemia (GVL) effect. Non-HLA determinants, such as immunomodulatory cytokines can promote or protect against GVHD. Certain cytokine gene polymorphisms have been associated with acute GVHD in related and unrelated donor HCT. Methods: 17 patients (pts) who underwent related or unrelated donor HCT for hematologic malignancies and their donors were retrospectively analyzed for polymorphisms in gene sequences for interleukin (IL)-6, IL-10, tumor necrosis factor-alpha (TNF-α), transforming growth factor-beta (TGF-β) and interferon gamma (IFN-γ) using SSP-PCR reagents from One Lambda Inc. (Canaga Park, CA, USA). Pts and donors were categorized into low, intermediate or high producers of respective cytokines based on single nucleotide polymorphisms (SNPs) identified by sequence specific primers as per manufacturer’s instructions. Conditioning regimens included tacrolimus/sirolimus or alemtuzumab/cyclosporine. Results: A marginal association was found between development of acute GVHD and donor intermediate producers of TGF-β (p=0.056). None of the other cytokine gene polymorphisms tested showed significant relationships to either acute or chronic GVHD. Of seven pts tested who received alemtuzumab conditioning, only one pt developed GVHD; both pt and donor were high producers of all five cytokine genes tested. Conclusions: These results suggest that TGF-β gene polymorphisms may affect risk of developing acute GVHD following allogeneic HCT. Further study is warranted in larger cohorts with measurement of low, intermediate, and high cytokine producers, as well as evaluation of the interplay of cytokines and alemtuzumab in GVHD.
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Kim, Jee Youn, Yeon Jin Kim, Hwa Sun Ryu, Hyung Sook Kim, Eunmiri Roh, Hwan Mook Kim, Jong Soon Kang, Jin Tae Hong, Youngsoo Kim, and Sang-Bae Han. "Kamebakaurin inhibits lipopolysaccharide-induced dendritic cell maturation by blocking transforming growth factor-beta activated kinase 1 (116.30)." Journal of Immunology 186, no. 1_Supplement (April 1, 2011): 116.30. http://dx.doi.org/10.4049/jimmunol.186.supp.116.30.
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Abstract Transforming growth factor-beta activated kinase-1 (TAK-1) is a serine/threonine kinase in the mitogen-activated protein kinase kinase kinase family. Once activated, TAK-1 will activate p38, JNK, and IKK, followed by activation of transcription factors AP-1 and NF-κB. Due to its role in the regulation of cell survival, differentiation, and inflammation, TAK-1 becomes one of the important drug targets in many human diseases. In this study, we show that TAK-1 can be directly inhibited by natural compound, kamebakaurin. Kamebakaurin inhibited the production of nitric oxide, IL-12, TNF-α, and IL-1β by dendritic cells, but did not affect their maturation process. We also showed that kamebakaurin inhibited the phosphorylation of p38 and JNK, but not ERK, in LPS-treated DCs. Kamebakarin also inhibited the phosphorylation of MEK3/6, upstream kinase of p38, and MKK4/7, upstream kinase of JNK, but not MEK1/2, upstream kinase of ERK. In addition, kamebakaurin inhibited NF-κB pathway, sequentially IKK phosphorylation, IκB-α degradation and nuclear translocation of NF-κB p65. Finally, we proved that kamebakaurin directly blocked autophosphorylation and kinase activity of TAK-1. Taken together, we show that kamebakaurin is a direct inhibitor of TAK-1 and suggest that it might be candidate for the treatment of inflammatory diseases.
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Salib, Rami J. "Transforming Growth Factor-β Gene Expression Studies in Nasal Mucosal Biopsies in Naturally Occurring Allergic Rhinitis." Annals of The Royal College of Surgeons of England 89, no. 6 (September 2007): 563–73. http://dx.doi.org/10.1308/003588407x202164.
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Introduction Evidence has been provided of enhanced epithelial transforming growth factor-beta (TGF-β) immunoreactivity in allergic rhinitis, including correlation with intra-epithelial mast cell numbers, and the co-localisation of TGF-β receptors to mast cells, suggesting that the epithelial expression of TGF-β may represent an important biological process involved in either the recruitment or retention of mast cells within the epithelium in naturally occurring allergic rhinitis. Patients and Methods In order to extend the above findings, evaluation was undertaken in whole nasal biopsies from subjects with naturally occurring allergic rhinitis, of levels of TGF-β isotypes and receptors gene expression using real-time quantitative polymerase chain reaction (TaqMan RT-PCR), and the results compared to those for tumour necrosis factor-alpha (TNF-α), as a positive control. The study was also extended to evaluate gene expression for connective tissue growth factor (CTGF) and Smad proteins, as downstream markers of TGF-β bioactivity, in the same populations. Results There were no significant differences between the rhinitic and non-rhinitic groups in the expression of TGF-β isoforms or Smad-3, Smad-6 and Smad-7 proteins; however, there was increased gene expression for TGF-βRI and TGF-βRII along with CTGF in seasonal allergic rhinitis. TNF-α gene expression was also increased in seasonal allergic rhinitis, consistent with a more acute inflammatory response in this form of rhinitis. Conclusions This study advances our understanding of the role of TGF-β in the pathogenesis of the inflammatory response in allergic rhinitis.
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LAHA, DIPRANJAN. "Abstract 5796: Targeting poorly differentiated and anaplastic thyroid cancer microenvironment via TNF-α/TGF-β/LOX signaling to improve drug delivery and treatment efficacy." Cancer Research 82, no. 12_Supplement (June 15, 2022): 5796. http://dx.doi.org/10.1158/1538-7445.am2022-5796.
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Abstract A major limitation of current systemic solid cancer therapies is the failure to effectively deliver drugs to cancer cells. Solid tumors have high cell density and poor lymphatic drainage, leading to higher interstitial fluid pressure (IFP). We previously showed that the tumor microenvironment of poorly-differentiated (PDTC) and anaplastic thyroid cancer (ATC) can be selectively and effectively treated with nanomedicine carrying recombinant human Tumor Necrosis Factor α (TNFα)(CYT6091), resulting in vascular leakage, decreased IFP, and increased intratumoral concentration of paclitaxel in vivo. The purpose of this study is to investigate the mechanisms involved in a TNFα-induced reduction of IFP. We investigated the effects of TNF-α on cytokines and extracellular matrix (ECM) proteins in tumor microenvironment. Our data showed that TNFα treatment downregulated transforming growth factor-beta (TGF-β) and Lysyl oxidase (LOX) and upregulated several ECM proteins. However, we observed LOX upregulation when we treated thyroid cancer with siTNF-α-receptor 1 or 2 followed by TNF-α, suggesting the involvement of TNF-α-receptors in treatment resistance. In addition to the role of LOX in stiffening the ECM, causing a barrier to drug delivery, we showed overexpression of LOX in aggressive thyroid cancer. We observed increased vascular leakage in siLOX-treated thyroid cancer xenografts, mimicking the effect of CYT-6091. Furthermore, we confirmed that the LOX expression in thyroid cancer is positively associated with transforming growth factor receptor 1 (TGFBR1). In TCGA thyroid cancer database the mRNA expression of TGFBR1 was positively correlated with those of ECM regulatory genes (ITGB2, ITGA2 and COL1A1) which were downregulated with TNF-α treated thyroid cancer cells. To assess the role of TGF-β on vascular permeability, we found that the TGF-β inhibitor (SB-431542) induced in vitro vascular leakage, while the recombinant TGF-β reversed TNF-α-induced in vitro vascular leakage in HUVEC cells. SB-431542 and TGF-β neutralizing antibodies independently and markedly improved treatment efficacy of paclitaxel in in vitro thyroid cancer 3D tumor spheroids. Moreover, TGF-β1 inhibition downregulates the protein levels of Smad3 molecules in thyroid cancer cells. TCGA database studies of thyroid cancer patient samples showed that SMAD3 positively correlated with TGFBR1 and LOX, suggesting the involvement of SMAD3 in TGF-β/LOX signaling in the TME. Citation Format: DIPRANJAN LAHA. Targeting poorly differentiated and anaplastic thyroid cancer microenvironment via TNF-α/TGF-β/LOX signaling to improve drug delivery and treatment efficacy [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 5796.
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Dei, A. A., B. I. Geltser, M. V. Antonyuk, T. A. Gvozdenko, E. P. Kalinina, and I. N. Titorenco. "Assessing the relationship of respiratory muscle strength and cytokine status in patients with community-acquired pneumonia." PULMONOLOGIYA 31, no. 3 (June 10, 2021): 311–19. http://dx.doi.org/10.18093/0869-0189-2021-31-3-311-319.
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Aim. Assessment of the role of cytokine-mediated changes in the development of respiratory muscle (RM) dysfunction in patients with community-acquired pneumonia (СAP). Methods. 84 men aged 18 – 26 years with a median of age 19.5 [18.4; 22.8]. Mild to moderate CAP (MCAP) was diagnosed in 62 (73.8%) patients and severe (SCAP) in 22 (26.2%). The expiratory (MEP, MRPDout) and inspiratory (MIP, MRPDin. SNIP) strength indices of RM were recorded on a MicrоRPM apparatus (CareFusion, UK). The severity of endogenous intoxication was verified using the following indices: hematologic (HII), leukocyte (LII), and nuclear. Serum concentrations of interleukins-2, -8, -10, basic fibroblast growth factor, transforming growth factor-beta, tumor necrosis factor-alpha (TNF-α), and a soluble receptor for TNF-α. Data processing was performed by cluster and correlation analysis methods. Results. Three clusters of patients with CAP were identified by the characteristic combinations of indicators of RM strength, endogenous intoxication, and cytokine status. The first cluster had MCAP, the second – both MCAP and SCAP, the third – SCAP. In the first cluster, dysfunction of expiratory RM prevailed, and in the second and third – dysfunction of inspiratory RM. In the midst of CAP, significant negative correlations of RM strength indicators with LII, HII, TNF-α, IL-10, IL-8, and IL-2 levels were recorded. The endogenous intoxication indices reached control values in all patients during recovery. The first cluster showed a decrease in the level of analyzed cytokines against isolated dysfunction of expiratory RM. The second cluster showed a tendency toward restoration of TNF-α and IL-8 levels, and only their SNIP index was normal. The third cluster showed minimal medians of RM strength against the continuing imbalance in the profile of pro- and anti-inflammatory cytokines during recovery. Conclusion. RM dysfunction in CAP is associated with cytokine-mediated dysfunction. The degree of cytokine involvement in this process depends on the severity of endogenous intoxication and the volume of alveolar inflammation.
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Liu, Yan, Hui Zhao, Jie Zhang, Ping Zhang, Ming Li, Fang Qi, Yizhou Wang, Shuang Kou, Qi Zheng, and Lei Wang. "The Regulatory Effect of Liuwei Dihuang Pills on Cytokines in Mice with Experimental Autoimmune Encephalomyelitis." American Journal of Chinese Medicine 40, no. 02 (January 2012): 295–308. http://dx.doi.org/10.1142/s0192415x12500231.
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The regulatory effect of Liuwei Dihuang Pills (LDP) was studied on cytokines in mice with experimental autoimmune encephalomyelitis (EAE), a model for human multiple sclerosis (MS), induced by immunization with MOG35-55 and complete Freund's adjuvant (CFA) supplemented with pertussis toxin (PTX). LDP was administrated orally for 40 days, and prednisone acetate (PA) was used as a control. The pathological changes in the spinal cords of mice were observed by light microscope with hematoxylin-eosin (HE) staining and transmission electron microscope (TEM). The protein and mRNA expression of tumor necrosis factor-alpha (TNF-α) and transforming growth factor-beta (TGF-β) in the spinal cords were assessed by immunohistochemistry and RT-PCR assay, and the cyclic adenosine monophosphate (cAMP) in mice plasma was measured by radioimmunoassay (RIA) on days 12, 25 and 40 post-immunization (PI). The results showed that inflammatory cells, demyelination and axonal loss were reduced, and that the protein and mRNA expression of TNF-α and the ratio of TNF-α/TGF-β were obviously decreased, to different extents. However, the levels of cAMP were enhanced in LDP-treated groups. These findings suggested that LDP regulates the cytokine balance in favor of T helper 1 (Th1)/regulatory T (Treg) cells, which depend on enhancement of cAMP levels. LDP has a potential role in the treatment of MS and other demyelinating diseases of the central nervous system.
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Yeung, Kam C., David W. Rose, Amardeep S. Dhillon, Diane Yaros, Marcus Gustafsson, Devasis Chatterjee, Brian McFerran, James Wyche, Walter Kolch, and John M. Sedivy. "Raf Kinase Inhibitor Protein Interacts with NF-κB-Inducing Kinase and TAK1 and Inhibits NF-κB Activation." Molecular and Cellular Biology 21, no. 21 (November 1, 2001): 7207–17. http://dx.doi.org/10.1128/mcb.21.21.7207-7217.2001.
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ABSTRACT The Raf kinase inhibitor protein (RKIP) acts as a negative regulator of the mitogen-activated protein (MAP) kinase (MAPK) cascade initiated by Raf-1. RKIP inhibits the phosphorylation of MAP/extracellular signal-regulated kinase 1 (MEK1) by Raf-1 by disrupting the interaction between these two kinases. We show here that RKIP also antagonizes the signal transduction pathways that mediate the activation of the transcription factor nuclear factor kappa B (NF-κB) in response to stimulation with tumor necrosis factor alpha (TNF-α) or interleukin 1 beta. Modulation of RKIP expression levels affected NF-κB signaling independent of the MAPK pathway. Genetic epistasis analysis involving the ectopic expression of kinases acting in the NF-κB pathway indicated that RKIP acts upstream of the kinase complex that mediates the phosphorylation and inactivation of the inhibitor of NF-κB (IκB). In vitro kinase assays showed that RKIP antagonizes the activation of the IκB kinase (IKK) activity elicited by TNF-α. RKIP physically interacted with four kinases of the NF-κB activation pathway, NF-κB-inducing kinase, transforming growth factor beta-activated kinase 1, IKKα, and IKKβ. This mode of action bears striking similarities to the interactions of RKIP with Raf-1 and MEK1 in the MAPK pathway. Emerging data from diverse organisms suggest that RKIP and RKIP-related proteins represent a new and evolutionarily highly conserved family of protein kinase regulators. Since the MAPK and NF-κB pathways have physiologically distinct roles, the function of RKIP may be, in part, to coordinate the regulation of these pathways.
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Ferreira, Joana, Mariana Oliveira, Manuel Bicho, and Fátima Serejo. "Role of Inflammatory/Immune Response and Cytokine Polymorphisms in the Severity of Chronic Hepatitis C (CHC) before and after Direct Acting Antiviral (DAAs) Treatment." International Journal of Molecular Sciences 24, no. 2 (January 10, 2023): 1380. http://dx.doi.org/10.3390/ijms24021380.
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Host regulatory immune response is involved in the hepatic inflammatory process caused by the hepatitis C virus (HCV). We aimed to determine if HCV clearance with direct-acting antivirals (DAAs) changes the hepatic fibrosis stage, biochemical parameters of liver injury, and inflammatory/immune responses. Sample: 329 chronic hepatitis C (CHC) patients, 134 of them treated with DAAs. Liver fibrosis was evaluated by transient elastography (FibroScan), biochemical and cellular parameters were determined by standard methods, cytokine concentration by enzyme-linked immunoabsorbent assay (ELISA), and genetic polymorphisms by polymerase chain reaction—restriction fragment length polymorphism (PCR-RFLP) or endpoint genotyping. Before DAA treatment, severe fibrosis or cirrhosis (F3/4) was associated with higher values of tumor necrosis factor-alpha (TNF-α) and genotypes transforming growth factor-beta-509 C/T_CC (TGF-β-509 C/T_CC), interleukine-10-1082 T/C_CC (IL-10-1082 T/C_CC), and IL-10-592 G/T_GT. After DAA treatment, fewer F3/4 patients and lower values of TNF-α were found. Patients with TNF-α-308 G/A_GG and IL-10-592 G/T_GT were at risk for F3/4. Lack of improvement of liver fibrosis was associated with lower baseline values of platelet count for genotypes TNF-α-308 G/A_GG and haplotype TT/GG of IL-10-1082 T/C and IL-10-592 G/T. Our study showed decreased liver fibrosis/inflammation and normalization of liver injury biomarkers after DAA treatment. It also points to the importance of suppressing the pro-inflammatory response by DAAs in the resolution of hepatitis C, contributing to the improvement of liver damage evaluated by transient elastography.
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Pervov, Yury, Anna Golitsina, Yuri Yugay, and Elena Markelova. "SALIVA CYTOKINE PROFILE IN MUCOSAAL IMMUNE DISTURBANCE IN PATIENTS WITH CHRONIC GENERALIZED PERIODONTITIS AND TYPE II DIABETES MELLITUS." Actual problems in dentistry 18, no. 4 (February 15, 2023): 62–67. http://dx.doi.org/10.18481/2077-7566-2022-18-4-62-67.
Full textAbstract:
Subject. The subject of the study is the cytokine profile of saliva in violation of mucosal immunity in patients with chronic generalized periodontitis and concomitant type II diabetes mellitus.
Objectives. The goal was to assess local levels of cytokines: tumor necrosis factor-alpha (TNF-α), interferon-gamma (IFN-γ), transforming growth factor-beta 1 (TGF-β1), interleukin-4 (IL-4), interleukin-17 (IL-17) in patients with chronic generalized periodontitis without concomitant pathology (group I), with chronic generalized periodontitis and type II diabetes mellitus (group II), as well as in patients without signs of periodontitis, but with established type II diabetes mellitus ( III group).
Methodology. 126 patients were examined, including: 47 people – group I, 49 people – group II and 30 people – group III. The control group consisted of healthy volunteers (30 people). Patient saliva was used as the research material. The levels of the studied cytokines TNF-α, IFN-γ, TGF-β1, IL-4, IL-17 were determined by the sandwich variant of enzyme-linked immunosorbent assay using specific reagents from R&D Diagnostics Inc (USA).
Results. In patients of all studied groups, a significant increase in TNF-α, IFN-γ, IL-4 and IL-17 was found. In the group of patients with chronic periodontitis, a more pronounced increase in TNF-α, IFN-γ, TGF-β1 and IL-17, as well as an increase in the ratio of pro- and anti-inflammatory cytokines, was registered.
Conclusion. The data obtained can be considered as promising markers for the personification of the prognosis for the development of chronic generalized periodontitis in type II diabetes mellitus.
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Carmona, Jorge U., Catalina López, and Alejandro Ceballos-Márquez. "Temporal Release and Denature of Several Mediators in Pure Platelet-Rich Plasma and Temperature-Induced Platelet Lysates Derived from a Similar Bovine Platelet Concentrate." Veterinary Medicine International 2022 (September 23, 2022): 1–11. http://dx.doi.org/10.1155/2022/2609508.
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There is scarce information about bovine platelet-rich plasma/platelet-rich gel (PRP/PRG) and related hemocomponents (HCs), such as platelet lysates (PLs), including growth factor (GF) and cytokine concentrations, and how the stability of these biomolecules could be affected by time and temperature. This study aimed to evaluate the release and stability of transforming growth factor beta 1 (TGF-β1), interleukin 4 (IL-4), and tumor necrosis factor alpha (TNF-α) contained in bovine pure PRP (P-PRP) and temperature-induced PL (TIPL) coming from a similar platelet concentrate (PC) at 4 and 37°C at 3 and 96 h. Platelet concentrates (PCs) presented a 1.7-fold concentration of platelets (PLTs) with negligible counts of white blood cells (WBCs) when compared to the counts for these cells in whole blood. TGF-β1 concentrations were significantly lowest in plasma followed by TIPL, chemical-induced PL (CIPL), and P-PRP. IL-4 and TNF-α concentrations did not differ between HCs. TGF-β1 concentrations were negatively affected in P-PRPs stored at 4°C at 3 and 96 h, whereas those from P-PRP maintained at 37°C presented similar concentrations to TIPL stored at both temperatures over time. IL-4 and TNF-α concentrations were not affected by time or temperature in any of the HCs evaluated. Pure PRGs released additional quantities of GF and cytokines over time when compared with HCs stored over 96 h at 4 and 37°C. The method, either chemical or physical, used for platelet activation or damage produces a different GF and cytokine release pattern, which makes to each evaluated HCs different despite they come from a similar bovine PC. P-PRP activated with calcium gluconate and maintained at 37°C, which polymerizes in P-PRG, showed the best GF and cytokine release/denature profile compared with the rest of the HCs evaluated.
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Anuradha, Rajamanickam, Saravanan Munisankar, Yukthi Bhootra, Nathalla Pavan Kumar, Chandrakumar Dolla, Paul Kumaran, and Subash Babu. "Coexistent Malnutrition Is Associated with Perturbations in Systemic and Antigen-Specific Cytokine Responses in Latent Tuberculosis Infection." Clinical and Vaccine Immunology 23, no. 4 (February 10, 2016): 339–45. http://dx.doi.org/10.1128/cvi.00009-16.
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ABSTRACTMalnutrition, as defined by low body mass index (BMI), is a major risk factor for the development of active tuberculosis (TB), although the biological basis underlying this susceptibility remains poorly characterized. To verify whether malnutrition affects the systemic and antigen-specific cytokine levels in individuals with latent TB (LTB), we examined circulating and TB antigen-stimulated levels of cytokines in individuals with LTB and low BMI (LBMI) and compared them with those in individuals with LTB and normal BMI (NBMI). Coexistent LBMI with LTB was characterized by diminished circulating levels of type 1 (gamma interferon [IFN-γ] and tumor necrosis factor alpha [TNF-α]), type 2 (interleukin-4 [IL-4]), type 17 (IL-22), and other proinflammatory (IL-1α, IL-1β, and IL-6) cytokines but elevated levels of other type 2 (IL-5 and IL-13) and regulatory (IL-10 and transforming growth factor beta [TGF-β]) cytokines. In addition, LBMI with LTB was associated with diminished TB antigen-induced IFN-γ, TNF-α, IL-6, IL-1α, and IL-1β levels. Finally, there was a significant positive correlation between BMI values and TNF-α and IL-1β levels and a significant negative correlation between BMI values and IL-2, IL-10, and TGF-β levels in individuals with LTB. Therefore, our data reveal that latent TB with a coexistent low BMI is characterized by diminished protective cytokine responses and heightened regulatory cytokine responses, providing a potential biological mechanism for the increased risk of developing active TB.
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Rajan, Thangavelu Soundara, Francesca Diomede, Placido Bramanti, Oriana Trubiani, and Emanuela Mazzon. "Conditioned medium from human gingival mesenchymal stem cells protects motor-neuron-like NSC-34 cells against scratch-injury-induced cell death." International Journal of Immunopathology and Pharmacology 30, no. 4 (November 15, 2017): 383–94. http://dx.doi.org/10.1177/0394632017740976.
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Neuronal cell death is a normal process during central nervous system (CNS) development and is also involved in the death of motor neurons in diverse spinal motor neuron degenerative diseases. Here, we investigated the neuroprotective effect of secretory factors released from human gingival mesenchymal stem cells (hGMSCs) in mechanically injured murine motor-neuron-like NSC-34 cells. The cells were exposed to scratch injury and the markers for apoptosis and oxidative stress were examined. Immunocytochemistry results showed that proapoptotic markers cleaved caspase-3 and Bax were elevated while anti-apoptotic protein Bcl-2 was suppressed in scratch-injured NSC-34 cells. Oxidative stress markers SOD-1, inducible nitric oxide synthase (iNOS), Cox-2, and proinflammatory cytokine tumor necrosis factor alpha (TNF-α) were activated. Conditioned medium (CM) derived from hGMSCs (hGMSC-CM) significantly blocked the cell death by suppressing SOD-1, iNOS, TNF-α, cleaved caspase-3, and Bax. Bcl-2 and anti-inflammatory cytokine anti-interleukin 10 (IL-10) were increased in hGMSC-CM-treated injured cells. Moreover, hGMSC-CM treatment upregulated neurotrophins anti-brain-derived neurotrophic factor (BDNF) and NT3. Western blot data of hGMSC-CM revealed the presence of neurotrophins nerve growth factor (NGF), NT3, anti-inflammatory cytokines IL-10, and transforming growth factor beta (TGF-β), suggesting their positive role to elicit neuroprotection. Our results propose that hGMSC-CM may serve as a simple and potential autologous therapeutic tool to treat motor neuron injury.
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Balsano, Rita, Zita Kruize, Martina Lunardi, Annalisa Comandatore, Mara Barone, Andrea Cavazzoni, Andrea David Re Cecconi, et al. "Transforming Growth Factor-Beta Signaling in Cancer-Induced Cachexia: From Molecular Pathways to the Clinics." Cells 11, no. 17 (August 28, 2022): 2671. http://dx.doi.org/10.3390/cells11172671.
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Cachexia is a metabolic syndrome consisting of massive loss of muscle mass and function that has a severe impact on the quality of life and survival of cancer patients. Up to 20% of lung cancer patients and up to 80% of pancreatic cancer patients are diagnosed with cachexia, leading to death in 20% of them. The main drivers of cachexia are cytokines such as interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), macrophage inhibitory cytokine 1 (MIC-1/GDF15) and transforming growth factor-beta (TGF-β). Besides its double-edged role as a tumor suppressor and activator, TGF-β causes muscle loss through myostatin-based signaling, involved in the reduction in protein synthesis and enhanced protein degradation. Additionally, TGF-β induces inhibin and activin, causing weight loss and muscle depletion, while MIC-1/GDF15, a member of the TGF-β superfamily, leads to anorexia and so, indirectly, to muscle wasting, acting on the hypothalamus center. Against this background, the blockade of TGF-β is tested as a potential mechanism to revert cachexia, and antibodies against TGF-β reduced weight and muscle loss in murine models of pancreatic cancer. This article reviews the role of the TGF-β pathway and to a minor extent of other molecules including microRNA in cancer onset and progression with a special focus on their involvement in cachexia, to enlighten whether TGF-β and such other players could be potential targets for therapy.
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Taylor, D. J., J. M. Evanson, and D. E. Woolley. "Contrasting effects of the protein kinase C inhibitor, staurosporine, on cytokine and phorbol ester stimulation of fructose 2,6-bisphosphate and prostaglandin E production by fibroblasts in vitro. Comparative studies using interleukin-1α, tumour necrosis factor α, transforming growth factor β, interferon-γ and 12-O-tetradecanoylphorbol 13-acetate." Biochemical Journal 269, no. 3 (August 1, 1990): 573–77. http://dx.doi.org/10.1042/bj2690573.
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It is known that both interleukin-1 alpha (IL-1 alpha) and 12-O-tetradecanoylphorbol 13-acetate (TPA) promote increases in intracellular levels of the glycolytic regulatory metabolite fructose 2,6-bisphosphate [Fru(2,6)P2] and in the production of prostaglandin E (PGE) by subcultured rheumatoid synovial cells (RSC) and human dermal fibroblasts in vitro. We report here that the protein kinase C inhibitor staurosporine enhanced the IL-1 alpha-induced increase in [Fru(2,6)P2] and PGE production by RSC, whereas in similar concentrations (3-30 nM) this inhibitor decreased the TPA-induced stimulation of these parameters. Staurosporine produced a similar enhancement of the response to IL-1 alpha by normal human dermal fibroblasts. The increased PGE production provoked by tumour necrosis factor alpha (TNF alpha) in RSC was also augmented by staurosporine, but, in contrast, the increases in cellular [Fru(2,6)P2] induced by transforming growth factor beta (TGF beta) and interferon-gamma (IFN-gamma) were diminished. Thus the protein kinase C inhibitor staurosporine discriminates not only between the effects produced by IL-1 alpha and TPA, but also between those of IL-1 alpha and two other cytokines (but not between IL-1 alpha and TNF alpha). These findings suggest that IL-1 alpha and probably TNF alpha act via an intracellular mechanism different from that mediating the action of TPA, TGF-beta and IFN-gamma, and provide evidence that staurosporine is capable of amplifying the IL-1 signal.
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Arafat, Eetmad A., Rehab Elsayed Marzouk, Sally Abdallah Mostafa, and Walaa H. E. Hamed. "Identification of the Molecular Basis of Nanocurcumin-Induced Telocyte Preservation within the Colon of Ulcerative Colitis Rat Model." Mediators of Inflammation 2021 (July 29, 2021): 1–13. http://dx.doi.org/10.1155/2021/7534601.
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Background. Telocytes (TCs) are a distinct type of interstitial cells that play a vital role in the pathogenesis of ulcerative colitis and colonic tissue hemostasis. The aim of this study was to examine the effect of nanocurcumin (NC) on the morphometric and immunohistochemical characterization of TCs in the ulcerative colitis (UC) rat model. Methods. Forty rats were randomly divided into control, NC, UC, and UC+NC groups. At the end of the experiment, the colon was dissected and prepared for histopathological and immunohistochemical assessment. Tissue homogenates were prepared for real-time PCR assessment of interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and transforming growth factor-beta (TGF-β) gene expression. Our results revealed extensive mucosal damage with inflammatory cell infiltration, significant reduction of CD34, and vimentin immunostained TCs in the colon of the UC group with significant elevation of expression of IL-6, TNF-α, and TGF-β. The UC+NC-treated group revealed significant elevation of TC count compared to the UC group besides, a significant reduction of the three gene expression. Conclusion. NC successfully targeted the colonic tissue, improved the mucosal lesion, preserve TCs distribution, and count through its anti-inflammatory and fibrinolytic properties.
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Rama Iñiguez, S., M. A. Dea-Ayuela, J. A. Sanchez-Brunete, J. J. Torrado, J. M. Alunda, and F. Bolas-Fernández. "Real-Time Reverse Transcription-PCR Quantification of Cytokine mRNA Expression in Golden Syrian Hamster Infected with Leishmania infantum and Treated with a New Amphotericin B Formulation." Antimicrobial Agents and Chemotherapy 50, no. 4 (April 2006): 1195–201. http://dx.doi.org/10.1128/aac.50.4.1195-1201.2006.
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ABSTRACT A real-time quantitative reverse transcription-PCR assay was developed for the quantification of cytokine mRNA expression in the golden Syrian hamster Mesocricetus auratus infected with Leishmania infantum and treated with amphotericin B (AMB) formulated in microspheres made of human serum albumin (HSA). Treatment was administered intravenously on days 69, 71, and 73 postinfection (p.i.) with 107 metacyclic promastigotes, at doses of 2 and 40 mg/kg of AMB. High infection levels were recorded for untreated animals by day 76 p.i., with parasite loads always about 2 log10 per gram higher in the liver than in the spleen. Treatment was highly effective with both doses, but at 40 mg/kg, almost complete parasite elimination was achieved. mRNA expression of gamma interferon (IFN-γ) and, to a lesser extent, tumor necrosis factor alpha (TNF-α) and transforming growth factor beta (TGF-β) in spleen cells was up-regulated in most animals of the untreated group. The mRNA expression of interleukin-4 was strongly down-regulated in untreated as well as treated infected animals. Treatment with the lower dose of AMB-HSA down-regulated the mRNA expression of IFN-γ and TNF-α, with no effect on the deactivating cytokine TGF-β. In contrast, treatment with the higher dose (40 mg/kg) of the formulation caused moderate up-regulation of IFN-γ and TNF-α and strong suppression of TGF-β. Treatment of noninfected animals did not alter the cytokine expression pattern with regard to untreated controls. Our results suggest that treatment of L. infantum-infected Syrian hamsters with highly effective nontoxic doses of AMB-HSA causes deactivation of the anti-inflammatory cytokine TGF-β, which in turn results in up-regulation of the Th1 cytokines IFN-γ and TNF-α.
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Okamoto, Lillian L., Caleb C. Reichhardt, Sierra Lopez, Anthony F. Alberto, Reganne K. Briggs, Laura A. Smith, Fernanda Batistel, and Kara J. Thornton. "PSII-18 The effects of fish oil supplementation on markers of inflammation and skeletal muscle and adipose growth in pigs." Journal of Animal Science 99, Supplement_3 (October 8, 2021): 314–15. http://dx.doi.org/10.1093/jas/skab235.578.
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Abstract Omega-3 fatty acids have immunomodulatory and anti-inflammatory effects. The objective of this project was to determine the effects of fish oil, a source of omega-3 fatty acids, on genes involved in inflammation and growth of skeletal muscle tissue after an LPS challenge. Male Landrace-New Hampshire weaned piglets (BW 8.21±0.83 kg) were used in a randomized complete block design and assigned to two treatments: 1) basal diet (n=7) and 2) basal diet plus 3% fish oil added (n = 7). Treatments were fed for 35 d. On d 34, an LPS challenge was performed and 24 h later, piglets were euthanized and skeletal muscle samples were collected from the longissimus lumborum and biceps femoris. Total mRNA was isolated and markers of inflammation [cyclophilin (Cyclo), nuclear factor kappa beta subunit-1 (NF-kB), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6)], skeletal muscle growth [paired box transcription factor-7 (Pax7), myogenic factor-5 (Myf5), myoblast determination factor-1 (MyoD), myogenin (MyoG)] and adipose growth (peroxisome proliferator activated receptor (PPARy), leptin, and adiponectin) were analyzed. Cyclophilin abundance was increased (P = 0.03) in fish-oil piglets compared to control piglets. Other markers of inflammation (TNF-α, IL-6, NF-kB) were not affected (P > 0.05) by fish-oil supplementation. Abundance of Myf5 was lower (P = 0.03) in fish oil piglets than control piglets. Other myogenic regulatory factors (Pax7, MyoD, MyoG) were not (P > 0.05) altered by treatment. Abundance of PPARy, leptin or adiponectin was not affected (P > 0.05) by fish-oil supplementation. Muscle location influenced (P < 0.01) abundance of leptin and adiponectin, with abundance being higher in the biceps femoris than in the longissimus lumborum. No other genes analyzed were impacted by muscle location (P > 0.05). Our findings suggest that supplementation of omega-3 fatty acids via fish-oil may affect the inflammatory response and skeletal muscle growth. Further research is needed to evaluate the impact of these results on animal production.
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Okamoto, Lillian L., Caleb C. Reichhardt, Sierra Lopez, Anthony F. Alberto, Reganne K. Briggs, Laura A. Smith, Fernanda Batistel, and Kara J. Thornton. "PSII-18 The effects of fish oil supplementation on markers of inflammation and skeletal muscle and adipose growth in pigs." Journal of Animal Science 99, Supplement_3 (October 8, 2021): 314–15. http://dx.doi.org/10.1093/jas/skab235.578.
Full textAbstract:
Abstract Omega-3 fatty acids have immunomodulatory and anti-inflammatory effects. The objective of this project was to determine the effects of fish oil, a source of omega-3 fatty acids, on genes involved in inflammation and growth of skeletal muscle tissue after an LPS challenge. Male Landrace-New Hampshire weaned piglets (BW 8.21±0.83 kg) were used in a randomized complete block design and assigned to two treatments: 1) basal diet (n=7) and 2) basal diet plus 3% fish oil added (n = 7). Treatments were fed for 35 d. On d 34, an LPS challenge was performed and 24 h later, piglets were euthanized and skeletal muscle samples were collected from the longissimus lumborum and biceps femoris. Total mRNA was isolated and markers of inflammation [cyclophilin (Cyclo), nuclear factor kappa beta subunit-1 (NF-kB), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6)], skeletal muscle growth [paired box transcription factor-7 (Pax7), myogenic factor-5 (Myf5), myoblast determination factor-1 (MyoD), myogenin (MyoG)] and adipose growth (peroxisome proliferator activated receptor (PPARy), leptin, and adiponectin) were analyzed. Cyclophilin abundance was increased (P = 0.03) in fish-oil piglets compared to control piglets. Other markers of inflammation (TNF-α, IL-6, NF-kB) were not affected (P > 0.05) by fish-oil supplementation. Abundance of Myf5 was lower (P = 0.03) in fish oil piglets than control piglets. Other myogenic regulatory factors (Pax7, MyoD, MyoG) were not (P > 0.05) altered by treatment. Abundance of PPARy, leptin or adiponectin was not affected (P > 0.05) by fish-oil supplementation. Muscle location influenced (P < 0.01) abundance of leptin and adiponectin, with abundance being higher in the biceps femoris than in the longissimus lumborum. No other genes analyzed were impacted by muscle location (P > 0.05). Our findings suggest that supplementation of omega-3 fatty acids via fish-oil may affect the inflammatory response and skeletal muscle growth. Further research is needed to evaluate the impact of these results on animal production.
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Tsafack, Eric Gonzal, Marius Mbiantcha, Gilbert Ateufack, Stephanie Flore Djuichou Nguemnang, William Nana Yousseu, Albert Donatien Atsamo, Vanessa Matah Marthe Mba, Carine Flore Adjouzem, and Egbe Ben Besong. "Antihypernociceptive and Neuroprotective Effects of the Aqueous and Methanol Stem-Bark Extracts of Nauclea pobeguinii (Rubiaceae) on STZ-Induced Diabetic Neuropathic Pain." Evidence-Based Complementary and Alternative Medicine 2021 (February 2, 2021): 1–17. http://dx.doi.org/10.1155/2021/6637584.
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The greatest common and devastating complication of diabetes is painful neuropathy that can cause hyperalgesia and allodynia. It can disturb psychosocial functioning by increasing levels of anxiety and depression. This work was designed to evaluate the antihyperalgesic, antidepressant, and anxiolytic-like effects of the aqueous and methanol extracts of Nauclea pobeguinii stem-bark in diabetic neuropathy induced by streptozotocin in mice. Diabetic neuropathy was induced in mice by the intraperitoneal administration of 200 mg/kg streptozotocin (STZ) to provoke hyperglycemia. Nauclea pobeguinii aqueous and methanol extracts at the doses of 150 and 300 mg/kg were administered by oral route, and their effects were evaluated on antihyperalgesic activity (Von Frey filaments, hot plate, acetone, and formalin tests), blood glucose levels, body weight, serum, sciatic nerve proinflammatory cytokines (TNF-α, IL-1β, and IL-6) and sciatic nerve growth factor (IGF and NGF) rates, depression (open field test, forced swimming test, tail suspension test), and anxiety (elevated plus maze, light-dark box test, social interaction). Oral administration of Nauclea pobeguinii stem-bark aqueous and methanol extracts (150 and 300 mg/kg) produced antihyperalgesic, antidepressant, and anxiolytic-like effects in STZ-induced diabetic neuropathic mice. Extracts also triggered a decrease in glycaemia and increased body weight in treated animals. They also significantly ( p <0.001) reduced tumour necrosis factor alpha (TNF-α), interleukin-1 beta (IL-1β), and IL-6 and significantly ( p <0.001) increased nerve growth factor (NGF) and insulin-like growth factor (IGF) in sciatic nerves. The results of this study confirmed that Nauclea pobeguinii aqueous and methanol extracts possess antihyperalgesic, antidepressant, and anxiolytic activities and could be beneficial therapeutic agents.
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Figueiredo, Maria M., Beatriz Deoti, Izabela F. Amorim, Aldair J. W. Pinto, Andrea Moraes, Carolina S. Carvalho, Sydnei Magno da Silva, Ana C. B. de Assis, Ana M. C. de Faria, and Wagner L. Tafuri. "Expression of Regulatory T Cells in Jejunum, Colon, and Cervical and Mesenteric Lymph Nodes of Dogs Naturally Infected with Leishmania infantum." Infection and Immunity 82, no. 9 (June 16, 2014): 3704–12. http://dx.doi.org/10.1128/iai.01862-14.
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ABSTRACTUsing flow cytometry, we evaluated the frequencies of CD4+and CD8+T cells and Foxp3+regulatory T cells (Tregs) in mononuclear cells in the jejunum, colon, and cervical and mesenteric lymph nodes of dogs naturally infected withLeishmania infantumand in uninfected controls. All infected dogs showed chronic lymphadenitis and enteritis. Despite persistent parasite loads, no erosion or ulcers were evident in the epithelial mucosa. The colon harbored more parasites than the jejunum. Frequencies of total CD4+, total Foxp3, and CD4+Foxp3+cells were higher in the jejunum than in the colon. Despite negative enzyme-linked immunosorbent assay (ELISA) serum results for cytokines, levels of interleukin-10 (IL-10), gamma interferon (IFN-γ), transforming growth factor beta (TGF-β), and tumor necrosis factor alpha (TNF-α) were higher in the jejunum than in the colon for infected dogs. However, IL-4 levels were higher in the colon than in the jejunum for infected dogs. There was no observed correlation between clinical signs and histopathological changes or immunological and parasitological findings in the gastrointestinal tract (GIT) of canines with visceral leishmaniasis. However, distinct segments of the GIT presented different immunological and parasitological responses. The jejunum showed a lower parasite load, with increased frequencies and expression of CD4, Foxp3, and CD8 receptors and IL-10, TGF-β, IFN-γ, and TNF-α cytokines. The colon showed a higher parasite load, with increasing expression of IL-4.Leishmania infantuminfection increased expression of CD4, Foxp3, IL-10, TGF-β, IFN-γ, and TNF-α and reduced CD8 and IL-4 expression in both the jejunum and the colon.
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Bianchi, Renata Cristiane Gennari, Eduardo Rochete Ropelle, Carlos Kiyoshi Katashima, José Barreto Campello Carvalheira, Luiz Roberto Lopes, and Nelson Adami Andreollo. "Analysis of the physical activity effects and measurement of pro-inflammatory cytokines in irradiated lungs in rats." Acta Cirurgica Brasileira 27, no. 3 (March 2012): 223–30. http://dx.doi.org/10.1590/s0102-86502012000300004.
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PURPOSE: To study if the pre-radiotherapy physical activity has radio-protective elements, by measuring the radio-induced activation of pro-inflammatory cytokines as interleukin-6 (il-6), transforming growth factor -β (tgf -β), tumor necrosis factor -α (tnf-α) and protein beta kinase β (ikkβ), through western blotting analysis. METHODS: A randomized study with 28 Wistar hannover rats, males, with a mean age of 90 days and weighing about 200 grams. The animals were divided into three groups: (GI, GII and GIII). GIII group were submitted to swimming for eight weeks (zero load, three times a week, about 30 minutes). Then, the groups (except the control group) were submitted to irradiation by cobalt therapy, single dose of 3.5 gray in the whole body. All animals were sacrificed by overdose of pentobarbital, according to the time for analysis of cytokines, and then a fragment of the lower lobe of the right lung went to western blotting analysis. RESULTS: The cytokines IKK β, TNF-α and IL-6 induced by radiation in the lung were lower in the exercised animals. However, exercise did not alter the radiation-induced increase in tgf-β. CONCLUSION: The results show a lower response in relation to inflammatory cytokines in the group that practiced the exercise pre-radiotherapy, showing that exercise can protect tissues from tissue damage due to irradiation.
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Leepiyasakulchai, Chaniya, Lech Ignatowicz, Andrzej Pawlowski, Gunilla Källenius, and Markus Sköld. "Failure To Recruit Anti-Inflammatory CD103+Dendritic Cells and a Diminished CD4+Foxp3+Regulatory T Cell Pool in Mice That Display Excessive Lung Inflammation and Increased Susceptibility to Mycobacterium tuberculosis." Infection and Immunity 80, no. 3 (January 3, 2012): 1128–39. http://dx.doi.org/10.1128/iai.05552-11.
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Susceptibility toMycobacterium tuberculosisis characterized by excessive lung inflammation, tissue damage, and failure to control bacterial growth. To increase our understanding of mechanisms that may regulate the host immune response in the lungs, we characterized dendritic cells expressing CD103 (αEintegrin) (αE-DCs) and CD4+Foxp3+regulatory T (Treg) cells duringM. tuberculosisinfection. In resistant C57BL/6 and BALB/c mice, the number of lung αE-DCs increased dramatically duringM. tuberculosisinfection. In contrast, highly susceptible DBA/2 mice failed to recruit αE-DCs even during chronic infection. Even though tumor necrosis factor alpha (TNF-α) is produced by multiple DCs and macrophage subsets and is required for control of bacterial growth, αE-DCs remained TNF-α negative. Instead, αE-DCs contained a high number of transforming growth factor beta-producing cells in infected mice. Further, we show that Tregcells in C57BL/6 and DBA/2 mice induce gamma interferon during pulmonary tuberculosis. In contrast to resistant mice, the Tregcell population was diminished in the lungs, but not in the draining pulmonary lymph nodes (PLN), of highly susceptible mice during chronic infection. Tregcells have been reported to inhibitM. tuberculosis-specific T cell immunity, leading to increased bacterial growth. Still, despite the reduced number of lung Tregcells in DBA/2 mice, the bacterial load in the lungs was increased compared to resistant animals. Our results show that αE-DCs and Tregcells that may regulate the host immune response are increased inM. tuberculosis-infected lungs of resistant mice but diminished in infected lungs of susceptible mice.
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Liu, BoTong, QiuHua Zhang, Xiao Wu, YanJun Fu, Hui Wang, YunXia Guan, ShiCheng Yang, YiLan Liu, WenCong Cao, and Jian Wang. "Effect of Bletilla striata on the Prevention of Postoperative Peritoneal Adhesions in Abrasion-Induced Rat Model." Evidence-Based Complementary and Alternative Medicine 2019 (June 10, 2019): 1–10. http://dx.doi.org/10.1155/2019/9148754.
Full textAbstract:
Postoperative peritoneal adhesions (PPAs) constitute a common complication of abdominal surgery with a high incidence. Bletilla striata (BS) is an important hemostatic drug used in China for nearly 2000 years. The purpose of this study was to investigate the effect of Bletilla striata on postoperative intestinal adhesion in rats. PPA was induced by cecal wall abrasion, and Bletilla striata was injected to observe its effect on adhesion in rats. The adhesion and inflammation score were assessed through visual observation and histopathologic evaluation. The levels of interleukin-1 (IL-1β), tumor necrosis factor (TNF-α), and interleukin-17F (IL-17F) in abdominal cavity and interleukin-6 (IL-6) in plasma were measured by enzyme-linked immunosorbent assay (ELISA) at 6 hours, 12 hours, 24 hours, and 1 week after operation. The tissue level of transforming growth factor beta-1 (TGF-β1) was also determined by ELISA on the seventh day after surgery. The expressions of collagen and TNF-α were, respectively, detected by Masson trichrome staining and immunohistochemical staining. The expression of TGF-β1 and alpha smooth muscle actin (α-SMA) was detected by Western blot. The result showed that Bletilla striata has obvious preventive effect on PPAs and celiac inflammation of PPAs. Bletilla striata could significantly reduce the level of IL-17F abdominal cavity and IL-6 in plasma. Masson trichrome staining and immunohistochemical staining results showed that Bletilla striata also decreased the expression of TNF-α and collagen. Western blot results showed that Bletilla striata decreased the expression of α-SMA and TGF-β1. Our results suggest that Bletilla striata decreased the development of abdominal adhesion in abrasion-induced model of rats and reduced the expression of the important substance which increased in PPAs. Bletilla striata can be further studied as a new and cheaper antiadhesive substance.
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Deng, Yufeng, Weizhou Li, Yingying Zhang, Jingjing Li, Fangting He, Ke Dong, Zehui Hong, Ruocheng Luo, and Xiaofang Pei. "α-Linolenic Acid Inhibits RANKL-Induced Osteoclastogenesis In Vitro and Prevents Inflammation In Vivo." Foods 12, no. 3 (February 3, 2023): 682. http://dx.doi.org/10.3390/foods12030682.
Full textAbstract:
Inflammation is an important risk factor for bone-destroying diseases. Our preliminary research found that Zanthoxylum bungeanum seed oil (ZBSO) is abundant in unsaturated fatty acids and could inhibit osteoclastogenesis in receptor activator of nuclear factor κB ligand (RANKL)-induced RAW264.7 cells. However, the key constituents in ZBSO in the prevention of osteoclastogenesis and its possible mechanism related to inflammation are still unclear. Therefore, in this study, oleic acid (OA), linoleic acid (LA), palmitoleic acid (PLA), and alpha-linolenic acid (ALA) in ZBSO, havingthe strongest effect on RANKL-induced osteoclastogenesis, were selected by a tartrate-resistant acid phosphatase (TRAP) staining method. Furthermore, the effects of the selected fatty acids on anti-inflammation and anti-osteoclastogenesis in vitro and in vivo were assessed using RT-qPCR. Among the four major unsaturated fatty acids we tested, ALA displayed the strongest inhibitory effect on osteoclastogenesis. The increased expression of free fatty acid receptor 4 (FFAR4) and β-arrestin2 (βarr2), as well as the decreased expression of nuclear factor-kappa B (NF-κB), tumor necrosis factor-α (TNF-α), nuclear factor of activated T-cells c1 (NFATc1), and tartrate-resistant acid phosphatase (TRAP) in RAW264.7 cells after ALA treatment were observed. Moreover, in ovariectomized osteoporotic rats with ALA preventive intervention, we found that the expression of TNF-α, interleukin-6 (IL-6), interleukin-1β (IL-1β), NFATc1, and TRAP were decreased, while with the ALA therapeutic intervention, downregulated expression of NF-κB, NFATc1, TRAP, and transforming growth factor beta-activated kinase 1 (TAK1) were noticed. These results indicate that ALA, as the major unsaturated fatty acid in ZBSO, could inhibit RANKL-induced osteoclastogenesis via the FFAR4/βarr2 signaling pathway and could prevent inflammation, suggesting that ZBSO may be a promising potential natural product of unsaturated fatty acids and a dietary supplement for the prevention of osteoclastogenesis and inflammatory diseases.
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Mazur, T., N. Demikhova, T. Rudenko, A. Yurchenko, O. Yezhova, S. Bokova, and A. Demikhov. "Chronic inflammation and progression of chronic kidney disease in patients with type 2 diabetes." Ukrainian Journal of Nephrology and Dialysis, no. 4(72) (December 12, 2021): 36–43. http://dx.doi.org/10.31450/ukrjnd.4(72).2021.05.
Full textAbstract:
Chronic inflammation, atherosclerosis, tubulointerstitial fibrosis, and vascular damage play a crucial role in the progression of chronic kidney disease (CKD) in patients with type 2 diabetes mellitus (DM). However, specific biomarkers that can determine the progression of diabetic kidney disease, including patients with minimal albuminuria, remain undefined.
The present study aimed to determine markers of chronic inflammation as indicators of CKD progression in patients with type 2 DM.
Methods. 45 patients with type 2 DM and stage 1-3 CKD were involved in this cross-sectional observational study. Analysis of cellular mechanisms of CKD progression was performed on the concentrations of endothelin-1 (ET-1), fibronectin (FN), tumor necrosis factor-alpha (TNF-α), transforming growth factor beta-1 (TGF-β1), and monocyte chemoattractant protein (MCP) -1) in the serum.
Results. In patients with type 2 DM, an increasing trend in the majority of endothelial and proinflammatory mediators was found according to the CKD stages despite normal albuminuria.
Conclusions. Concentrations of TNF-α, ET, TGF-β1 and MCP-1 can be used to assess the progression of CKD in patients with type 2 DM with normal albuminuria. Further researches are needed to determine early indicators of diabetic kidney disease progression.
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Thackray, Alana M., Andrew N. McKenzie, Michael A. Klein, Angus Lauder, and Raymond Bujdoso. "Accelerated Prion Disease in the Absence of Interleukin-10." Journal of Virology 78, no. 24 (December 15, 2004): 13697–707. http://dx.doi.org/10.1128/jvi.78.24.13697-13707.2004.
Full textAbstract:
ABSTRACT The identity of pro- and anti-inflammatory cytokines in the neuropathogenesis of prion diseases remains undefined. Here we have investigated the role of anti-inflammatory cytokines on the progression of prion disease through the use of mice that lack interleukin-4 (IL-4), IL-10, IL-13, or both IL-4 and IL-13. Collectively our data show that among these anti-inflammatory cytokines, IL-10 plays a prominent role in the regulation of prion disease. Mice deficient in IL-10 are highly susceptible to the development of prion disease and show a markedly shortened incubation time. In addition, we have correlated cytokine gene expression in prion-inoculated IL-10−/− mice to wild-type-inoculated animals. Our experiments show that in the absence of IL-10 there is an early expression of tumor necrosis factor alpha (TNF-α). In wild-type prion-inoculated mice, the expression of TNF-α mRNA occurs at a later time point that correlates with the extended incubation time for terminal disease development in these animals compared to those that lack IL-10. Elevated levels of IL-13 mRNA are found at early time points in the central nervous system of prion-inoculated IL-10−/− mice. At terminal disease, the brains of wild-type mice inoculated with RML or ME7 are characterized by elevated levels of mRNA for the proinflammatory cytokines TNF-α and IL-1β, together with the anti-inflammatory cytokines IL-10, IL-13, and transforming growth factor beta. Our data are consistent with a role for proinflammatory cytokines in the initiation of pathology during prion disease and an attempt by anti-inflammatory cytokines to regulate the ensuing, invariably fatal pathology.