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Littérature scientifique sur le sujet « Trasforming Growth Factor Beta TNF-α »

Auteur : Grafiati

Publié le 9 mars 2023

Mis à jour le 10 mars 2023

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Articles de revues sur le sujet "Trasforming Growth Factor Beta TNF-α"

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 та 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, № 1 (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, et al. "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 (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, et al. "Disturbance of Tumor Necrosis Factor Alpha-Mediated Beta Interferon Signaling in Cervical Carcinoma Cells." Journal of Virology 76, no. 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 та ін. "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 та Jingxin Cao. "Vaccinia Virus E3 Suppresses Expression of Diverse Cytokines through Inhibition of the PKR, NF-κB, and IRF3 Pathways". Journal of Virology 83, № 13 (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 та 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, № 2 (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 (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 (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 та 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, № 8 (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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Thèses sur le sujet "Trasforming Growth Factor Beta TNF-α"

LOCATELLI, LUIGI. "Expression of aVB6 integrin by Pkhd1-defective cholangiocytes links enhanced ductal secretion of Macrophage chemokines to progressive portal fibrosis in Congenital Hepatic Fibrosis." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2013. http://hdl.handle.net/10281/41733.

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BACKGROUND AND AIMS: Congenital Hepatic Fibrosis (CHF) is caused by mutations in PKHD1, a gene encoding for fibrocystin, a protein of unknown function, expressed in cholangiocyte cilia and centromers. In CHF, biliary dysgenesis is accompanied by severe progressive portal fibrosis and portal hypertension. The mechanisms responsible for portal fibrosis in CHF are unclear. The αvβ6 integrin mediates local activation of TGFβ1 and is expressed by reactive cholangiocytes during cholestasis. To understand the mechanisms of fibrosis in CHF we studied the expression of αvβ6 integrin and its regulation in Pkhd1del4/del4 mice. METHODS: In Pkhd1del4/del4 mice we studied, at different ages (1-12 months): a) portal fibrosis (Sirius Red) and portal hypertension (spleen weight/body weight); b) αvβ6 mRNA and protein expression (RT-PCR, IHC); c) α-SMA and TGFβ1 mRNA expression (RT-PCR); d) portal inflammatory infiltrate (IHC for CD45 and FACS analysis of whole liver infiltrate); f) cytokines secretion from cultured monolayers of primary cholangiocytes (Luminex assay); g) cytokine effects on monocyte/macrophage proliferation (MTS assay) and migration (Boyden chamber); h) TGFβ1 and TNFα effects on β6 integrin mRNA expression by cultured cholangiocytes before and after inhibition of the TGFβ receptor type II (TGFβRII); i) TGFβ1 effects on collagen type I (COLL1) mRNA expression by cultured cholangiocytes. RESULTS: Pkhd1del4/del4 mice showed a progressive increase in αvβ6 integrin expression on biliary cyst epithelia. Expression of αvβ6 correlated with portal fibrosis (r=0.94, p<0.02) and with enrichment of a CD45+ve cell infiltrate in the portal space (r=0.97, p<0.01). Gene expression of TGFβ1 showed a similar age-dependent increase. FACS analysis showed that 50-75% of the CD45+ve cells were macrophages (CD45/CD11b/F4/80+ve). Cultured polarized Pkhd1del4/del4 cholangiocytes secreted from the basolateral side significantly increased amounts of CXCL1 and CXCL10 (p<0.05). Both cytokines were able to stimulate macrophage migration (p<0.05). Basal expression of β6 mRNA by cultured Pkhd1del4/del4 cholangiocytes (0.015±0.002 2^-dCt) was potently stimulated by the macrophage-derived cytokines TGFβ1 (0.017±0.002 2^-dCt, p<0.05) and TNFα (0.018±0.003 2^-dCt, p<0.05). Inhibition of TGFβRII completely blunted TGFβ1 (0.014±0.003 2^-dCt, p<0.05) but not TNFα effects (0.017±0.001 2^-dCt, p=ns) on β6 mRNA. COLL1 mRNA expression by cultured Pkhd1del4/del4 cholangiocytes (0.0009±0.0003 2^-dCt) was further and significantly increased after TGFβ1 stimulation (0.002±0.0005 2^-dCt, p<0.05). CONCLUSIONS: Pkhd1del4/del4 cholangiocytes possess increased basolateral secretory functions of chemokines (CXCL1, CXCL10) able to orchestrate macrophage homing to the peribiliary microenvironment. In turn, by releasing TGFβ1 and TNFα, macrophages up-regulate αvβ6 integrin in Pkhd1del4/del4 cholangiocytes. αvβ6 integrin activates latent TGFβ1, further increasing the fibrogenic properties of cholangiocytes.

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Kam, Siu-kei Christy, та 甘笑琪. "The role of TGF-{221} signaling in the initiation of TNF-α expression in human PBMC derived macrophages". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B38746049.

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Freese, Christiane [Verfasser]. "Rolle der Plasmakonzentrationen von transforming growth factor-β1 [factor-beta1] (TGFβ1) [TGF beta 1], {Tumor necrosis factor α [Tumor necrosis factor alpha] {(TNF α) [TNF alpha] und Plasminogen-Activator-Inhibitor-(PAI-)-Antigen bei Patienten mit Diabetes Mellitus Typ 2 und koronarer Herzkrankheit / vorglegt von Christiane Freese". 2002. http://d-nb.info/97149200X/34.

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Suntharalingam, Gaayathiri. "Der Einfluss der Induktion von Tumornekrosefaktor α und Transforming-Growth-Factor β auf die epithelial-mesenchymale Transition oraler Plattenepithelkarzinome im CAM-Assay". Doctoral thesis, 2021. http://hdl.handle.net/21.11130/00-1735-0000-0005-1567-0.

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Chapitres de livres sur le sujet "Trasforming Growth Factor Beta TNF-α"

El-Youssef, M., A. Hughes, K. J. Bloch, S. R. Martin, and P. R. Harmatz. "Identification of tumor necrosis factor alpha (TNF-α) and transforming growth factor beta (TGF-β) in murine milk." In Advances in Mucosal Immunology. Springer Netherlands, 1990. http://dx.doi.org/10.1007/978-94-009-1848-1_162.

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Lambert, Charles. "Attenuating Cancer Cachexia-Prolonging Life." In Frailty and Sarcopenia - Recent Evidence and New Perspectives. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.101250.

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Death by cancer cachexia is dependent on the time allotted to cancer to cause muscle and fat wasting. If clinicians, nurses, researchers can prolong the life of a cancer patient other therapeutic interventions such as radiation and chemotherapy may be given the time to work and rid the cancer patient of tumors and save lives. Three areas by which cancer induces cachexia is through impaired insulin-like growth factor signaling, elevations in the proinflammatory cytokines TNF-α and IL-6 and subsequent reductions in muscle protein synthesis and increases in muscle protein degradation. Therefore, it is important to augment the IGF-1 signaling, block TNF-α and IL-6 in cancer cachexia and in other ways augment muscle protein synthesis or decrease muscle protein degradation. Ghrelin like growth hormone secretagogues, monoclonal antibodies to TNF-α and IL-6, testosterone, and anabolic steroids, the beta 2 agonist albuterol, resistance exercise, and creatine monohydrate (with resistance exercise) are beneficial in increasing muscle protein synthesis and/or reducing muscle protein breakdown. With these muscle augmenting agents/interventions, the duration that a cancer patient lives is prolonged so that radiation and chemotherapy as well as emerging technologies can rid the cancer patient of cancer and save lives.

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