Academic literature on the topic 'Pro-inflammatory cytokine TNF -α'
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Journal articles on the topic "Pro-inflammatory cytokine TNF -α"
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Dumaine, Jennifer E., and Noah T. Ashley. "Acute sleep fragmentation does not alter pro-inflammatory cytokine gene expression in brain or peripheral tissues of leptin-deficient mice." PeerJ 6 (February 19, 2018): e4423. http://dx.doi.org/10.7717/peerj.4423.
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Obesity and sleep fragmentation (SF) are often co-occurring pro-inflammatory conditions in patients with obstructive sleep apnea. Leptin is a peptide hormone produced by adipocytes that has anorexigenic effects upon appetite while regulating immunity. The role of leptin in mediating inflammatory responses to SF is incompletely understood. Male C57BL/6j (lean) and ob/ob mice (leptin-deficient mice exhibiting obese phenotype) were subjected to SF or control conditions for 24 h using an automated SF chamber. Trunk blood and tissue samples from the periphery (liver, spleen, fat, and heart) and brain (hypothalamus, prefrontal cortex, and hippocampus) were collected. Quantitative PCR was used to determine relative cytokine gene expression of pro-inflammatory (IL-1β, TNF-α) and anti-inflammatory (TGF-β1) cytokines. Enzyme-linked immunosorbent assay (ELISA) was used to determine serum corticosterone concentration. Ob/ob mice exhibited elevated cytokine gene expression in liver (TNF-α, TGF-β1), heart (TGF-β1), fat (TNF-α), and brain (hippocampus, hypothalamus, prefrontal cortex: IL-1β, TNF-α) compared with wild-type mice. Conversely, leptin deficiency decreased pro-inflammatory cytokine gene expression in heart (IL-1β, TNF-α). SF significantly increased IL-1β and TNF-α gene expression in fat and TGF-β1 expression in spleen relative to controls, but only in wild-type mice. SF increased basal serum corticosterone regardless of genotype. Taken together, these findings suggest that leptin deficiency affects cytokine gene expression differently in the brain compared to peripheral tissues with minimal interaction from acute SF.
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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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Paramalingam, Sivalingam Suppiah, Julian Thumboo, Sheila Vasoo, Szu Tien Thio, Connie Tse, and Kok-Yong Fong. "In vivo Pro- and Anti-inflammatory Cytokines in Normal and Patients with Rheumatoid Arthritis." Annals of the Academy of Medicine, Singapore 36, no. 2 (February 15, 2007): 96–99. http://dx.doi.org/10.47102/annals-acadmedsg.v36n2p96.
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Introduction: Rheumatoid arthritis (RA) is a chronic, deforming arthritis that can lead to disabilities and poor quality of life. Cytokines are protein mediators of inflammation and are produced as a result of the activation of various cellular reactions. They are the final mediators and/or regulators of the inflammatory process. Materials and Methods: The sera from 64 RA patients were assayed for both Th-1 and Th-2 related cytokines and soluble TNF-α receptors (IFN-γ, TGF-β, TNF-α, IL-1β, IL-2, IL-4, IL-6, IL-8, IL-10, IL-12, IL-18, sTNF-R1 and sTNF-R2) using ELISA. Results: The pro-inflammatory cytokines (IL-1, IL-6, IL-8, IL-18 and TNF-α) were significantly elevated in RA patients, while TGF-β, an immunomodulatory cytokine, was elevated in control individuals. When the RA patients were categorised as active or inactive based on DAS scores, similar cytokines profiles were observed in both RA sub-groups. However, assays of sTNF-R1 and sTNFR-2 were noted to be significantly elevated in inactive RA patients when compared to active patients. Conclusion: Our findings indicate that local production of cytokine inhibitors is capable of diminishing disease activity and cytokine activity. Key words: Cytokines, Inflammation, Rheumatoid arthritis soluble receptors
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Pakdemirli, Ahu, and Gizem Calibasi Kocal. "TNF-alpha Induces Pro-Inflammatory Factors in Colorectal Cancer Microenvironment." Medical Science and Discovery 7, no. 4 (April 30, 2020): 466–69. http://dx.doi.org/10.36472/msd.v7i4.368.
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Objective: The tumor microenvironment has a crucial role in organizing cancer malignancy, progression, drug resistance and survival. It consists of cellular and non-cellular components. These non-cellular components such as cytokines, extracellular matrix, growth factors and metabolites are responsible for shifting the action from pro-cancer to anti-cancer effects. Twenty percent of all cancers occur in association with chronic inflammation via cytokines. Even cancers that are not caused by chronic inflammation, present high levels of cytokine expression pattern in their tumor microenvironment. Tumor necrosis factor-alpha (TNF-α) and some interleukins are characterized as pro-tumorigenic cytokines and they were involved in cancer by presenting their ability to activate the oncogenic transcription factors. The aim of this study is to evaluate the remodeling of colorectal cancer tumor microenvironment by TNF-α.
Material and Methods: TNF-α (5ng/ml) was applied to HT-29 colorectal cancer cells, then human soluble factors were determined by using Human Cytokine Group 1, 8 plex Panel (Bio-Rad Laboratories Inc. USA) and Magpix Luminex instrument and xPONENT software (version 4.2, Luminex Corp, Austin, Texas, US). The results were normalized to total protein concentration estimated via Bradford assay.
Results: Current research highlights the effect of TNF-α on the tumor microenvironment. Interleukin-6 and interleukin -8 soluble factors were higher in TNF-α treated colorectal cancer cells when compared with untreated control group.
Conclusion: The results of the study show that TNF-α is responsible for elevating the levels of interleukin-6 and interleukin-8, which are associated with inflammation in the tumor microenvironment.
Key words: Colorectal Cancer, Tumor Microenvironment, Cytokines, TNF-α, Interleukin-6, interleukin -8
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Musa, Fauzia, Nathan Shaviya, Fidelis Mambo, Collins Abonyo, Erick Barasa, Philemon Wafula, George Sowayi, Mustafa Barasa, and Tom Were. "Cytokine profiles in highly active antiretroviral treatment non-adherent, adherent and naive HIV-1 infected patients in Western Kenya." African Health Sciences 21, no. 4 (December 14, 2021): 1584–92. http://dx.doi.org/10.4314/ahs.v21i4.12.
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Background: Cytokines play an important role in signaling the immune system to build an adequate immune responseagainst HIV. HIV distorts the balance between pro and anti-inflammatory cytokines causing viral replication. Highly active antiretroviral treatment (HAART) acts by trying to restore pro and anti-inflammatory cytokine balance. It is not clear how HAART non-adherence influences circulating cytokine levels. This study therefore determined cytokine levels in HAART non-adherent individuals.
Methods: This cross-sectional study recruited 163 participants (51 controls, 23 HIV-1+ HAART naive, 28 HAART-adherent6 months, 19 HAART-adherent 12 months and 42 HAART non-adherent). Cytokines were analyzed by ELISA while CD4 T cells determined in 3.0 μl of whole blood using BD FACSCaliburTM and viral load in 0.2ml plasma sample using Abbott Molecular m2000sp sample preparation and m2000rt real-time amplification and detection systems (Abbott MolecularInc., Illinois, USA) according to the manufacturer’s methods.
Results: IL-4, IL-6, IL-10, TNF-α and TGF-β were significantly elevated in HIV-1 HAART non-adherent compared withHIV-1 HAART adherent and healthy controls P<0.01. IFN- γ was significantly decreased in HIV-1 HAART non-adherentcompared with HIV-1 HAART adherent and healthy controls P<0.01. TNF-α and TGF-β were significantly reduced in HIV-1 HAART adherent patients at 12 months compared to those at 6 months P<0.01. IL-4 and IL-10 correlated positively withviral load. IL-4, IL-6, IL-10, TNF-α and TGF- β associated inversely with CD4 T cell counts and body mass index (BMI).
Conclusion: This study established that HAART adherence is immunologically beneficial to the pro and anti-inflammatory cytokine balance milieu while non-adherence appears to cause alterations in pro and anti-inflammatory cytokines warping the balance in this dichotomy.
Keywords: Cytokines; non-adherence; HAART.
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Sutcigil, Levent, Cagatay Oktenli, Ugur Musabak, Ali Bozkurt, Adnan Cansever, Ozcan Uzun, S. Yavuz Sanisoglu, et al. "Pro- and Anti-Inflammatory Cytokine Balance in Major Depression: Effect of Sertraline Therapy." Clinical and Developmental Immunology 2007 (2007): 1–6. http://dx.doi.org/10.1155/2007/76396.
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The specific associations between antidepressant treatment and alterations in the levels of cytokines remain to be elucidated. In this study, we aimed to explore the role of IL-2, IL-4, IL-12, TNF-α, TGF-β1, and MCP-1 in major depression and to investigate the effects of sertraline therapy. Cytokine and chemokine levels were measured at the time of admission and 8 weeks after sertraline treatment. Our results suggest that the proinflammatory cytokines (IL-2, IL-12, and TNF-α) and MCP-1 were significantly higher, whereas anti-inflammatory cytokines IL-4 and TGF-β1 were significantly lower in patients with major depression than those of healthy controls. It seems likely that the sertraline therapy might have exerted immunomodulatory effects through a decrease in the proinflammatory cytokine IL-12 and an increase in the anti-inflammatory cytokines IL-4 and TGF-β1. In conclusion, our results indicate that Th1-, Th2-, and Th3-type cytokines are altered in the depressed patients and some of them might have been corrected by sertraline treatment.
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McGeehan, Gerard M., and Joanne Uhl. "TNF-α in Human Diseases." Current Pharmaceutical Design 2, no. 6 (December 1996): 662–67. http://dx.doi.org/10.2174/1381612802666221004191458.
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TNF-α is a potent pro-inflammatory cytokine produced primarily by monycytes and macrophages. Excessive or prolonged production of TNF-α has been implicated in inflammatory processes as well as in the pathogenesis of other human diseases. There are a number of strategies for inhibiting TNF-α activity ranging from transcriptional events to neutralization of the soluble cytokine. Several of these approaches are being pursued in the clinic, suggesting that some novel, anti-cytokine agents may come to the market in the near future.
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Нlushchenko, T. A. "Investigation of the Cytokine Spectrum of Patients' Oral Fluid with Generalized Periodontitis and Metabolic Syndrome." Ukraïnsʹkij žurnal medicini, bìologìï ta sportu 7, no. 1 (March 22, 2022): 208–12. http://dx.doi.org/10.26693/jmbs07.01.208.
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The purpose of the study was to study the state of cytokine regulation of oral fluid in patients with generalized periodontitis and metabolic syndrome. Materials and methods. For this study, 3 groups of surveys were formed. The main group included 30 people with generalized periodontitis on the background of metabolic syndrome; 30 people with generalized periodontitis, without somatic pathology, formed a comparison group. The obtained results were compared with the data of 20 practically healthy individuals with intact periodontium who were included in the control group. The content of pro-inflammatory cytokines IL-1β, IL-6, TNF-α and anti-inflammatory cytokines IL-4, TGF-β1 in the oral fluid of the study groups was determined by solid-phase enzyme-linked immunosorbent assay. Results and discussion. According to the research, on average, the highest levels of pro-inflammatory cytokines (IL-1β, IL-6, TNF-α) were observed in patients with periodontal disease on the background of metabolic syndrome. We investigated increase in the concentration of proinflammatory IL-1β. The average value of IL-6 in the oral fluid of patients with metabolic syndrome exceeded this figure in persons not burdened with somatic pathology by 1.3 times, the difference with healthy individuals was more significant: the indicators differed by 2 times. That can be considered an immune response to the inflammatory process in periodontal tissues. The next stage is the beginning of the cytokine cascade, which is characterized by increased production of IL-6 and TNF-α – inducers of acute phase protein synthesis. TNF-α causes an increase in the number of free radicals and can lead to intensification of apoptosis. Due to the fact that anti-inflammatory IL-4 blocks the induced expression of pro-inflammatory IL-6 and TNF-α, a decrease in its level in oral fluid can be considered an unfavorable factor in the course of inflammatory-dystrophic periodontal lesions in patients with syndrome X. Given that TGF-β1 is an immunosuppressive factor, a decrease in its concentration indicates a deficiency of local factors of immune protection in patients with periodontal disease on the background of metabolic syndrome. Conclusion. Patients with metabolic syndrome and periodontal disease have significant disorders of cytokine regulation, which are complicated by age: expression of proinflammatory IL-1β, IL-6, TNF-α on the background of reduced anti-inflammatory cytokines IL-4 and TGF-β1. Such changes in cytokine homeostasis indicate chronic inflammation, insufficient efficiency of regenerative processes in tooth-retaining tissues, and, as a consequence, lead to a more severe course of periodontal disease in people with metabolic syndrome
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Mourouzis, Konstantinos, Evangelos Oikonomou, Gerasimos Siasos, Sotiris Tsalamadris, Georgia Vogiatzi, Alexios Antonopoulos, Petros Fountoulakis, Athina Goliopoulou, Spyridon Papaioannou, and Dimitris Tousoulis. "Pro-inflammatory Cytokines in Acute Coronary Syndromes." Current Pharmaceutical Design 26, no. 36 (October 23, 2020): 4624–47. http://dx.doi.org/10.2174/1381612826666200413082353.
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Background: Over the last decades, the role of inflammation and immune system activation in the initiation and progression of coronary artery disease (CAD) has been established. Objectives: The study aimed to present the interplay between cytokines and their actions preceding and shortly after ACS. Methods: We searched in a systemic manner the most relevant articles to the topic of inflammation, cytokines, vulnerable plaque and myocardial infarction in MEDLINE, COCHRANE and EMBASE databases. Results: Different classes of cytokines (intereleukin [IL]-1 family, Tumor necrosis factor-alpha (TNF-α) family, chemokines, adipokines, interferons) are implicated in the entire process leading to destabilization of the atherosclerotic plaque, and consequently, to the incidence of myocardial infarction. Especially IL-1 and TNF-α family are involved in inflammatory cell accumulation, vulnerable plaque formation, platelet aggregation, cardiomyocyte apoptosis and adverse remodeling following the myocardial infarction. Several cytokines such as IL-6, adiponectin, interferon-γ, appear with significant prognostic value in ACS patients. Thus, research interest focuses on the modulation of inflammation in ACS to improve clinical outcomes. Conclusion: Understanding the unique characteristics that accompany each cytokine-cytokine receptor interaction could illuminate the signaling pathways involved in plaque destabilization and indicate future treatment strategies to improve cardiovascular prognosis in ACS patients.
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Stumpf, Christian, Sebastian Petzi, Katrin Seybold, Gerald Wasmeier, Martin Arnold, Dorette Raaz, Atilla Yilmaz, Werner G. Daniel, and Christoph D. Garlichs. "Atorvastatin enhances interleukin-10 levels and improves cardiac function in rats after acute myocardial infarction." Clinical Science 116, no. 1 (November 28, 2008): 45–52. http://dx.doi.org/10.1042/cs20080042.
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LV (left ventricular) remodelling is the basic mechanism of HF (heart failure) following MI (myocardial infarction). Although there is evidence that pro-inflammatory cytokines [including TNF-α (tumour necrosis factor-α) and IL-6 (interleukin-6)] are involved in the remodelling process, only little is known about the role of anti-inflammatory cytokines, such as IL-10. As accumulating evidence has revealed that statins possess anti-inflammatory properties, the aim of the present study was to elucidate the effect of atorvastatin on the modulation of the anti-inflammatory cytokine IL-10 and its effect on LV function in rats with HF subsequent to MI. Rats with MI, induced by permanent LAD (left anterior descending) branch coronary artery ligation, were treated for 4 weeks with atorvastatin (10 mg·kg−1 of body weight·day−1 via oral gavage) starting on the first day after induction of MI. Cardiac function was assessed by echocardiography and cardiac catheterization 4 weeks after MI induction. Membrane-bound and soluble fractions of TNF-α, IL-6 and IL-10 protein, the TNF-α/IL-10 ratio, serum levels of MCP-1 (monocyte chemoattractant protein-1) as well as myocardial macrophage infiltration were analysed. Treatment with atorvastatin significantly improved post-MI LV function (fractional shortening, +120%; dP/dtmax, +147%; and LV end-diastolic pressure, −27%). Furthermore atorvastatin treatment markedly decreased the levels of TNF-α, IL-6 and MCP-1, reduced myocardial infiltration of macrophages and significantly increased myocardial and serum levels of the anti-inflammatory cytokine IL-10. Thus the balance between pro-inflammatory and anti-inflammatory cytokines was shifted in the anti-inflammatory direction, as shown by a significantly decreased TNF-α/IL-10 ratio. Atorvastatin ameliorated early LV remodelling and improved LV function in rats with HF subsequent to MI. Our study suggests that the modulation of the balance between pro- and anti-inflammatory cytokines towards the anti-inflammatory cytokine IL-10 is one salutary mechanism underlying how atorvastatin influences post-MI remodelling and thus improves LV function.
Dissertations / Theses on the topic "Pro-inflammatory cytokine TNF -α"
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Michlewska, Sylwia. "Macrophage phagocytosis of apoptotic neutrophils is critically regulated by the opposing actions of pro-inflammatory and anti-inflammatory agents : key role for TNF-α." Thesis, University of Edinburgh, 2011. http://hdl.handle.net/1842/5594.
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Development of chronic inflammation or autoimmunity may be related to deregulated mechanisms orchestrating successful resolution of inflammation, especially apoptosis of inflammatory cells and their subsequent clearance by macrophages (Mφ). Chronically inflamed sites are characterised by an excess of the key pro-inflammatory cytokine tumor necrosis factor-α (TNF-α) and importantly, TNF-α inhibitors, widely used in the clinical setting for the treatment of rheumatoid arthritis (RA), inflammatory bowel disease and psoriasis, significantly delay disease progression. TNF-α therefore may affect processes implicated in resolution of inflammation. Although TNF-α and pro-inflammatory bacterial products such as lipopolysaccharide (LPS) influence rates of inflammatory cell apoptosis, little is known about their effects on Mφ phagocytosis of apoptotic cells (efferocytosis). In this PhD thesis, the effects of several pro-inflammatory agents (i.e., LPS, lipoteichoic acid (LTA), peptidoglycan (PGN) and TNF-α) on efferocytosis by human blood monocytederived Mφ (MDMφ) have been investigated. LPS, LTA and PGN all inhibited MDMφ efferocytosis in a concentration- and time-dependent manner; however, LPS did not inhibit the uptake of immunoglobulin-G (IgG)-opsonized erythrocytes. Moreover, although TNF-α did inhibit efferocytosis, phagocytosis of IgG-opsonized erythrocytes was not inhibited. Furthermore, the LPS effect was attenuated by dimeric soluble human recombinant TNF receptor-1 (sTNFR1/ Fc), indicating a critical role of TNF-α. Concomitant treatments with monomeric soluble human recombinant TNF receptor-1 (sTNF-R1) or the TNF-α Converting Enzyme (TACE) inhibitor, TOPI-0, only partially reversed the inhibitory effect of LPS. Even though TNF-α release takes place within the first few hours following LPS stimulation, the LPS-induced inhibitory effect occurred only if treatment was performed for 96 hours or longer. Analysis of supernatants obtained from LPS-treated MDMφ revealed that there appears to be interplay between concentrations of TNF-α and interleukin-10 (IL-10) and that these cytokines exert opposing actions on efferocytosis. IL-10 per se increased MDMφ efferocytosis and addition of exogenous IL-10 to LPS-treated samples rescued phagocytosis. The latter effect was associated with the IL-10-induced, concentration-dependent inhibition of TNF-α release. Interestingly, when IL-10 was added to TNF-α-treated MDMφ, only slight augmentation of phagocytosis was observed. Furthermore, when IL-10-mediated effects were blocked by concomitant treatment with anti-human IL-10 receptor 1 antibody (anti-IL-10- R1Ab), the LPS inhibitory effect on phagocytosis was much greater and occurred at 24 hours after treatment. The role of IL-10 on efferocytosis was also investigated using IL-10 deficient murine bone marrow-derived Mφ (BMDMφ). IL-10 deficient BMDMφ, when compared to wild-type, were characterised by a much lower ability to phagocytose apoptotic neutrophils and this effect was independent of culture conditions (control samples and LPS or TNF-α treatments). Finally, effects of the synthetic steroid (dexamethasone) and nonsteroidal anti-inflammatory drugs (NSAID) on MDMφ phagocytosis were examined. Dexamethasone, like IL-10, augmented MDMφ efferocytosis, reversed the inhibitory effects of both LPS and TNF-α, and suppressed LPS-induced production of TNF-α. In contrast NSAID did not increase MDMφ efferocytosis per se. However, preliminary data suggest that aspirin blocks the inhibitory effect of TNF-α on phagocytosis. In summary, it has been determined that prolonged treatment with proinflammatory agents such as LPS, LTA and PGN inhibits MDMφ efferocytosis which may potentially postpone the resolution of inflammation in vivo. I have shown that TNF-α is a key mediator in this process and that IL-10 exerts an important regulatory effect on TNF-α production and consequently on efferocytosis. Furthermore, several approaches have been unveiled to successfully reverse LPS-mediated inhibition of efferocytosis by decreasing either TNF-α production or its inhibitory effect with sTNF-RI/Fc, exogenous IL- 10 or dexamethasone. These findings indicate that TNF-α and other agents which influence efferocytosis may have significance in the resolution phase of inflammation. In addition, presented findings provide important mechanistic information into the potential mode of action of anti-TNF-α agents and steroids and may help to explain their clinical success in the treatment of chronic inflammatory diseases.
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Mejías, Luque Raquel. "Regulatory effects of pro-inflammatory cytokines on genes associated with gastric carcinogenesis." Doctoral thesis, Universitat Pompeu Fabra, 2009. http://hdl.handle.net/10803/7156.
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El patró específic d'expressió de glicosiltransferases i antígens Lewis observat a la mucosa gàstrica normal es perd durant el procés de la carcinogènesi gàstrica. Aquí descrivim que canvis en l'expressió dels antígens Lewis en cèl·lules HT-29/M3 de càncer de còlon induïts per la transfecció del cDNA de FUT1 resulten en un fenotip menys invasiu i menys metastàtic.La gastritis crònica produïda per la infecció per Helicobacter pylori és un dels principals determinants en la patogènesi del càncer gàstric, i comporta nivells elevats de citoquines proinflamatòries com TNF-α, IL-1β o IL-6, que poden regular l'expressió de gens implicats en la transformació neoplàsica gàstrica. Vam analitzar l'efecte de citoquines proinflamatòries en l'expressió de glicosiltransferases i antígens Lewis en cèl·lules de càncer gàstric va ser analitzat i vam observar que el tractament d'aquestes cèl·lules amb IL-1β augmentava l'expressió d'antígens Lewis de tipus 2. A més, vam observar que tumors gàstrics amb inflamació crònica presentaven nivells més elevats d'estructures glicosídiques de tipus 2, suggerint que determinades glicosiltransferases podrien estar regulades per la inflamació.
Els adenocarcinomes gàstrics de tipus intestinal s'originen a partir d'una sèrie successiva de lesions precanceroses que porten a una transdiferenciació intestinal de la mucosa gàstrica. En aquest procés s'activa l'expressió de diferents gens intestinals a les cèl·lules gàstriques, com és el cas dels gens de les mucines intestinals MUC2 i MUC4 i del factor de transcripció intestinal CDX2. Nosaltres vam estudiar l'efecte de citoquines inflamatòries i de les seves vies de senyalització associades en l'expressió d'aquests gens va ser estudiat. El primer que vam constatar va ser que IL-6 regulava l'expressió de MUC4 a través de la via de gp130/STAT3 a línies cel·lulars de càncer gàstric, mentre que l'expressió de MUC2 era induïda per TNF-α a través de la via de senyalització de NF-κB. A més, vam observar que l'expressió de CDX2 no era regulada per citoquines inflamatòries. Finalment, vam trobar que les diferències en l'expressió de les mucines intestinals MUC2 i MUC4 a tumors gàstrics podien ser explicades per diferències en el tipus d'inflamació predominant.
De tots aquests resultats podem concloure que la inflamació i les vies de senyalització associades modulen l'expressió de gens associats a la carcinogènesi gàstrica.
In the gastric carcinogenetic process the specific expression pattern of glycosyltransferases and Lewis antigens displayed by the normal gastric mucosa is lost. We detected that changes in the expression of Lewis antigens induced by the transfection of FUT1 cDNA in HT-29/M3 cells determined a less invasive and metastatic phenotype.
Chronic gastritis caused by H. pylori infection is a major determinant in the pathogenesis of gastric cancer, and present increased levels of the pro-inflammatory cytokines TNF-α, IL-1β and IL-6, which can regulate the expression of genes involved in the gastric neoplastic transformation. We analysed the effect of pro-inflammatory cytokines on the expression of glycosyltransferases and Lewis antigens in gastric cancer cells. IL-1β treatment increased the expression of type 2 Lewis antigens, and, in addition, we observed that gastric tumours with chronic inflammation displayed increased levels of type 2 glycan structures, suggesting that specific glycosyltransferases may be regulated by inflammation.
Intestinal-type gastric adenocarcinomas develop from successive pre-cancerous lesions that lead to an intestinal transdifferentiation of the gastric mucosa. In this process many intestinal genes are activated in gastric cells, such as the intestinal mucin MUC2 and MUC4 genes and the transcription factor CDX2. We studied the effect of pro-inflammatory cytokines and their associated signalling pathways on the expression of these genes. IL-6 regulated the expression of MUC4 through the gp130/STAT3 signalling pathway in gastric cancer cell lines, while MUC2 expression was induced by TNF-α through the NF-κB signalling pathway. No effects on CDX2 expression were observed after cytokine treatment in gastric tumour cells. Finally, we found that the differences observed in the expression of the intestinal mucins MUC2 and MUC4 in gastric tumours could be explained by differences in the predominant type of inflammation present in gastric adenocarcinomas.
In conclusion, our results suggest that inflammation and its associated signalling pathways modulate the expression of genes associated with gastric carcinogenesis.
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Grandjean-Laquerriere, Alexia. "Mécanismes de régulation de la production de cytokines pro-inflammatoires (TNF-α,IL-6,IL-)8 et IL-18 et anti-inflammatoire (IL-10) : modèle du kératinocyte humain irradié par des UVB/Alexia Grandjean." Reims, 2001. http://www.theses.fr/2001REIMP202.
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Les kératinocytes participent à la défense immunitaire de l'organisme en synthétisant de nombreuses cytokines. Nous avons étudié au cours de ce travail les mécanismes de régulation de la synthèse de cytokines pro-inflammatoires (TNF-a, IL-6, IL-8 et IL-18) et anti-inflammatoire (IL-10) dans des cultures de kératinocytes irradiés par un rayonnement UVB. Nous avons observé une augmentation dose-dépendante de l'expression des cytokines en fonction de la dose d'UVB appliquée. Nous avons ensuite cherché à définir l'implication des facteurs de transcription NF-kB et AP-1 dans la régulation de la synthèse de cytokines en utilisant la curcumine et le PDTC. En présence de curcumine, nous observons une inhibition de l'activation du facteur NF-kB et de la synthèse des cytokines inflammatoires. A l'opposé, l'expression de l'IL-10 est augmentée. En revanche, l'activation du facteur AP-1 n'est pas affectée par la curcumine. En présence de PDTC, nous observons une inhibition de l'activation du facteur NF-kB ainsi qu'une augmentation de l'activation du facteur AP-1 ; ainsi qu'une inhibition de l'expression du TNF-a et de l'IL-6 et une activation de l'IL-8 et de l'IL-10. Ces résultats suggèrent une régulation du TNF-a et de l'IL-6 NF-kB dépendante, et de l'IL-8 NF-kB et AP-1 dépendante. Puis nous avons étudié la voie de la PKA. Pour cela nous avons traité des kératinocytes irradiés avec: 1) dbAMPc, PGE2 et toxine cholérique (agents qui augmentent l'AMPc intracellulaire) et, 2) H89 et PKAi (inhibiteurs spécifiques). Nous observons, en présence des analogues de l'AMPc, une inhibition de l'expression du TNF-a et de l'IL-18 ainsi qu'une augmentation de l'IL-6 et de l'IL-10. Le traitement par les inhibiteurs de la PKA a pour conséquence une inhibition de la synthèse des quatre cytokines étudiées. Ces résultats montrent que la régulation des cytokines produites lors de l'irradiation des kératinocytes fait intervenir des voies de signalisation différentes selon la cytokine étudiée.
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Betina-Bencharif, Soumeya. "Isolement et caractérisation de saponosides extraits de deux plantes médicinales : Cyclamen africanum, Zygophyllum cornutum et évalution de leur activité anti-inflammatoire." Thesis, Dijon, 2014. http://www.theses.fr/2014DIJOPE03/document.
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L’apparition de plusieurs maladies, telles que le cancer, le diabète, l'hypertension artérielle et la propagation d'infections de type virus mutagènes peuvent être liées à la qualité et au mode de vie que nous menons aujourd’hui. En effet, plusieurs études sur les facteurs déclenchant ces maladies dites "morbides" à long ou à court terme, sont liées au stress et à la qualité des aliments consommés, qu'ils soient d'origine végétale ou animale. Ces maladies deviennent un phénomène courant, elles touchent différentes races et toutes les catégories de la société. D'après les recherches ethnobotaniques, les substances d’origine naturelle, ont permis à des civilisations de survivre à des maladies mortelles. A titre d'exemple, on retrouve ainsi des références à des périodes de fièvre paludique en Chine et à des symptômes de cette maladie dans le «Huangdi Neijiang» Le Canon de Médecine datant des environs du premier siècle avant notre ère, plus de 2000 ans, qui relate de l'emploi de plantes médicinales, pour soulager les fièvres (Desgrouas et al., 2014).Vers 186 avant J.-C. apparaît, dans certaines régions de Chine, l'utilisation en tisane, du Qing hao su, appelé plus tard artémisinine en Occident et extrait d'une plante médicinale utilisée comme antipyrétique appelée "Qing hao", Artemisia annua ou Armoise annuelle. L'artemisinine bloque une enzyme qui permet au parasite de pomper le calcium et l'empêche ainsi de se développer. Au jour d'aujourd'hui l’Artemisinin-based combination therapy, en français Thérapie combinée à base d'artémisinine et en sigle ACT, est une thérapie et une prévention tertiaire dans les cas de paludisme simple.Dans cette optique notre étude vient s'ajouter à une longue série d'études menées sur les plantes médicinales et les substances naturelles extraites. Elle a pour objectif de révéler de nouvelles biomolécules, de mettre en évidence leurs activités biologiques grâce à des techniques de biotechnologies d'une part. D'autre part ces investigations permettront de valoriser les ressources naturelles qui se distinguent par leur endémicité.Pour se faire, notre choix s'est porté sur deux plantes médicinales endémiques à l'Algérie Cyclamen africanum Boiss. & Reuter et Zygophyllum cornutum Coss. , après une recherche ethnobotanique sur la pharmacopée traditionnelle du Nord de l'Afrique, et qui a révélé l’efficacité de ces plantes dans les problèmes inflammatoires minimes chez les autochtones, nous avons entrepris des investigations pharmaco- biochimiques.Ces dernières nous ont permis d'isoler : cinq composés à partir de l'extrait méthanolique des racines de l'espèce Cyclamen africanum Boiss. & Reuter, deux nouvelles saponines triterpéniques de type Oleanane, Afrocyclamin A et B (1, 2), ainsi que trois saponines triterpénoïdes connus sous le nom de lysikokianoside (3), deglucocyclamin I (4) et de son dérivé d'acide dicrotalique (5); et Sept saponosides connus à partir de l'extrait méthanolique de la plante entière de Zygophyllum cornutum Coss., ces saponosides sont de type ursane, ce type de triterpène est rapporté dans cette espèce pour la première fois et peuvent être considérés comme un marqueur chimio-taxonomique (chemotype) du genre Zygophyllum. Les structures ont été élucidées, sur la base de l'analyse des spectres de l'expérience RMN-1D et RMN- 2D (COSY, TOCSY, NOESY, HMBC et HSQC) et spectrométrie de masse en source FAB mode ion négatif. Des activités biologiques, des fractions saponosidiques Fr.1 et Fr.2, ont été testées sur des lignées de Rats mâles et femelles, de la race Winstar pour évaluer l'activité anti inflammatoire.La fraction saponosidique Fr.1 de Cyclamen africanum à la dose 5 mg, a montré un effet significatif sur l'inflammation causé par la carragénine, en réduisant l'oedème et la réponse immunitaire, qui s'est traduite par la concentration des protéines de la réponse inflammatoire (PRI) à travers leurs action sur les pro-médiateurs de l'inflammation (COX-2, PGE2, TNF -α, iNOS)The appearance of several diseases, such as cancer, diabetes, high blood pressure and spread of infections mutagenic virus type can be linked to the quality and lifestyle that we lead today. Indeed, several studies on the factors triggering these so-called "morbid" long-or short-term illnesses are related to stress and quality of food consumed, whether of plant and animal origin. These diseases are becoming a common occurrence, they affect different races and all classes of society. According ethnobotanical research, naturally occurring substances, allowed civilizations to survive deadly diseases. For example, we thus find references to periods of malarial fever in China and one of the symptoms of this disease in the "Huangdi Neijiang" The Canon of Medicine dating from around the first century BC, more than 2000 years, which relates to the use of herbal medicines to relieve fevers (Desgrouas et al., 2014).Around 186 BC appears, in some parts of China, the use in herbal tea, Qing hao su, later known as artemisinin in the West and extracted from a medicinal plant used as antipyretic called "Qing hao" Artemisia annua or annual wormwood. Artemisinin blocks an enzyme which enables the parasite to pump calcium and prevents it from developing. As of today the Artemisinin-based combination therapy in French Combination therapy of artemisinin and ACT acronym, is a therapy and tertiary prevention in cases of uncomplicated malaria.From this perspective our study adds to a long series of studies on medicinal plants and natural substances extracted. It aims to reveal new biomolecules, highlighting their biological activities through techniques of biotechnology on the one hand. Moreover, these investigations will develop natural resources that are characterized by endemic.To do this, our choice is focused on two endemic medicinal plants in Algeria Cyclamen africanum Boiss. & Reuter and Zygophyllum cornutum Coss. After an ethnobotanical research on traditional medicine in Northern Africa, which showed the effectiveness of these plants in minimal inflammatory problems among Aboriginal, we undertook biochemical pharmacological investigations.The latter allowed us to isolate, five compounds from the methanol extract of the roots of the species Cyclamen africanum Boiss. Reuter & two new oleanane triterpene saponins type, Afrocyclamin A and B (1, 2) and three triterpenoid saponins known lysikokianoside of (3), deglucocyclamin I (4) and its derivative dicrotalique acid (5) September and known from the methanol extract saponins from the whole plant of Zygophyllum cornutum Coss. these saponins are ursane type, type triterpenes are reported in this species for the first time and can be considered a chemotherapy marker Taxonomic (chemotype) of Zygophyllum kind. The structures were elucidated on the basis of the analysis of NMR spectra of the experience-1D and 2D-NMR (COSY, TOCSY, NOESY, HSQC and HMBC) and mass spectrometry method negative ion FAB source. The biological activities of saponosidiques FR.1 and Fr.2 fractions were tested on lines of male and female rats of the Winstar rats to evaluate the anti-inflammatory activity. The saponosidique fraction FR.1 Cyclamen africanum the 5 mg dose, showed a significant effect on inflammation caused by carrageenan, reducing edema and immune response, which resulted in the concentration of protein the inflammatory response (PRI) through their action on the pro-inflammatory mediators (COX-2, PGE2, TNF -α, iNOS). The fraction of Fr.2 saponosidique Zygophyllum dose 20 mg did not show a significant effect on inflammation in general
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Österberg, Johanna. "Inflammatory Reactions in Peritonitis and Malignant Obstructive Jaundice : Clinical and Experimental Studies with Special Emphasis on the Cellular Immune Response." Doctoral thesis, Uppsala University, Department of Surgical Sciences, 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-4767.
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Patients with peritonitis or malignant obstructive jaundice (HPB+) have an increased morbidity and mortality due to sepsis. An altered cell-mediated immunity in the intestinal mucosa might promote gut barrier failure, increased endotoxin and cytokine release and bacterial translocation (BT) in these conditions. A clinically relevant rat model of polymicrobial peritonitis induced sepsis by cecal ligation and puncture (CLP) was used. Septic animals demonstrated a superficial injury in the small intestinal mucosa, and a significant reduction in T lymphocytes in the villi, as well as increased number of macrophages in the villi and in the MLNs as compared to sham. CLP caused increased concentration of TNF-α and IL-6 in ascitic fluid. CLP + the immunomodulator Linomide decreased the TNF-α level, reduced mucosal damage and attenuated the changes in T lymphocytes and macrophages observed following CLP. CLP + selective cyclooxygenase (COX)-2 inhibitor (SC-236) or nonselective COX inhibitor (indometacin) decreased the amount of macrophages in the mucosa and the MLNs compared to untreated CLP. CLP + indometacin decreased T lymphocytes in the villi and MLNs. SC-236 + CLP reduced mucosal injury and cytokine release as compared to indometacin. An increased rate of apoptosis in both the mucosa and MLNs was seen following CLP; COX inhibitors enhanced this phenomenon in the MLNs.
BT occurred infrequently in patients with acute peritonitis and in HPB+ there was no evidence of BT. Peritonitis and HPB+ causes significant inflammatory cellular reactions as increased endotoxin and cytokine plasma levels and an altered immune cell distribution in MLNs, in HPB+ a high rate of apoptosis in MLNs was observed.
An altered pattern of immunocompetent cells within the mucosa and in MLNs was found in experimental and clinical peritonitis as in HPB+. Lymphocyte depletion may be a result of increased apoptosis, which could reduce the ability of septic or jaundice patients to eradicate infection.
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Bollenbach, Maud. "Nouvelles cibles pour l'étude et le développement d'outils pharmacologiques originaux pour le traitement des douleurs neuropathiques." Thesis, Strasbourg, 2017. http://www.theses.fr/2017STRAF022.
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Les douleurs neuropathiques désignent une hypersensibilité du système nerveux central sensoriel. C’est une maladie chronique et handicapante qui touche environ 6% de la population française. Cependant, à l’heure actuelle, il n’existe pas de traitement spécifique et efficace. Dans le cadre de cette thèse, nous avons utilisé deux stratégies différentes afin de développer des outils pharmacologiques originaux pour traiter ces douleurs : une approche phénotypique autour de deux inhibiteurs de la surproduction de TNFα (un dérivé de 2-aminopyrimidine et un dérivé de pyridin-2-yl guanidine) et une approche moléculaire autour du MY 5445 (un inhibiteur de PDE5 dérivé de phtalazine). En particulier, notre travail s’est basé sur la conception, la synthèse et l’étude des relations structure-activité autour de ces différents hits et nous avons obtenu des composés efficaces par voie i.p. ou per-os sur un modèle murin de douleurs neuropathiques.En parallèle de ce travail de pharmacologie, nous avons développé différents systèmes catalytiques (Pd, Cu) en milieu micellaire afin de former des liaisons C-N à température quasi-ambianteNeuropathic pains correspond to a central sensory nervous system hypersensitivity. It is a chronic and disabling disease, which touch around 6% of the French population. Nowadays, there is no specific and efficient treatment. In my PhD project, we used two different strategies in order to develop innovative pharmacological tools to treat those pains: a phenotypic approach around two TNFα overproduction inhibitor (a 2-aminopyrimidine derivative and a pyridin-2-yl guanidine derivative) and a molecular approach around MY 5445 (a phthalazine PDE5 inhibitor). Our work was based on the design, synthesis and structure-activity relationship study around various hits and we obtained compounds i.p. and orally effective on a murin neuropathic pain model.In parallel to this pharmacological work, we developed different catalytic systems (Pd, Cu) under micellar conditions to form C-N bonds at almost room temperature
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Fotheringham, Julie A. "Regulation of the pro-inflammatory cytokine TNF-[alpha] by adenosine receptors in monocytes and macrophages." 2003. http://hdl.handle.net/1993/19851.
Full textBooks on the topic "Pro-inflammatory cytokine TNF -α"
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K. Gautam, Rupesh, Lokesh Deb, and Kamal Dua, eds. Natural Products for the Management of Arthritic Disorders. BENTHAM SCIENCE PUBLISHERS, 2022. http://dx.doi.org/10.2174/97898150507761220101.
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Rheumatoid arthritis (RA) is the most common inflammatory complication and affects approximately 1 % of the global population. It affects three times more women than men. RA is an autoimmune disorder elicited by exposure of genetic factors from the host to unknown antigens causing arthritogenic complaints. It also includes the activation of lymphocytes as well as CD4+ helper T cells along with local release of chronic inflammatory mediators and cytokines like tumor necrosis factor (TNF α) and various cytokines like interleukins (IL) that enormously affect the joints. The available allopathic therapies for RA are not a cure for the complications, and antibody therapy and surgical procedures are expensive. However, in the present era, researchers and healthcare professionals have moved toward natural medicines obtained from plants and other natural sources. Research based on developments in phytomedicine has progressed steadily. Evidence has been collected to show the massive therapeutic potential of medicinal plants used in various traditional systems against many pathological complications. Researchers have focused on the therapeutic potential of natural products used for treatment and counteracting various disorders along with their complications having negligible adverse effects. Natural Products for the Management of Arthritic Disorders compiles current knowledge about the bioactive compounds and herbal formulations useful in the treatment of rheumatoid arthritis. 11 chapters explain the role of natural products in the management of rheumatoid arthritis. Topics have been contributed by experts in medicinal chemistry and rheumatology. The book first introduces the reader to rheumatoid arthritis before delving into conventional and alternative therapies for the disease. The editors have also included special topics such as the biomarkers for RA, cytokines and anti-inflammatory mediators, preclinical and clinical studies. The range of topics should provide a comprehensive overview of natural remedies for arthritis and the role of natural products in anti-arthritic drug development. The information will be useful for many readers including medical and pharmacology students, multidisciplinary research scholars, scientists, pharma / herbal / food industrialists, and policy makers.
Book chapters on the topic "Pro-inflammatory cytokine TNF -α"
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Vogler, D., G. Schmittat, and S. Ohrndorf. "Rheumatism and wIRA Therapy." In Water-filtered Infrared A (wIRA) Irradiation, 225–32. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-92880-3_19.
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AbstractRheumatologic disorders comprise various conditions having different etiologies and pathogenesis, the leading clinical symptoms of which are chronic joint pain and musculoskeletal impairment. In the context of a multimodal therapy concept, the use of hyperthermia (HT) is a classical and developing adjuvant symptomatic treatment option. wIRA is an effective and well-established variant of thermal therapy in different rheumatologic disorders. This article summarizes the current state of research into locally applied wIRA in the field of rheumatism and rheumatological diseases.Local and serially applied wIRA significantly relieves pain in patients with axial spondyloarthritis (axSpA), osteoarthritis (OA) and fibromyalgia (FM), which, at least reduces the requirement for analgesics and has positive effects on well-being, functional status or disease activity. wIRA has been shown to reduce levels of C-reactive protein (CRP) and proinflammatory cytokine tumour necrosis factor α (TNFα). Given its safety and tolerability, wIRA is highly amenable in combination with standard therapies.Currently, wIRA effects are assessed in OA patients, non-inflammatory arthralgia and recent-onset arthritis of the hands. Preliminary data on effects on pain, global disease burden and functional status are promising. The potential value of wIRA, for e.g., Raynaud’s phenomena and sclerotic skin changes, need further evaluation.
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Bashir, Haamid, Mohammad Hayat Bhat, and Sabhiya Majid. "Molecular Pathogenesis of Inflammatory Cytokines in Insulin Resistance Diabetes Mellitus." In Insights on Antimicrobial Peptides [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.100971.
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Diabetes Mellitus Type 2 (T2DM) is a non-communicable and multifactorial disease. It is a leading cause of premature deaths worldwide. Inflammatory cytokines are reported that they have potential to enhance insulin resistance and hence T2DM. The current research was taken to investigate the possible role of inflammatory mediators: Tumor Necrosis Factor (TNF-α) and White blood cells (WBC’s) in mobilizing biological molecules mainly immunological nature. A total of 320 subjects were selected in this study among them 160 were T2DM cases and 160 were healthy controls. Serum concentration of Tumor Necrosis Factor-a (TNF-α) was quantified by ELISA method, WBC count was measured on Sysmax (Germany) hematology analyzer, biochemical and Immunoassay parameters were done on fully automatic analyzers. The expression of candidate pro-inflammatory cytokine (TNF-α), and (WBC’s) were elevated in T2DM. TNF-α shows association (p<0.001) with glycemic profile and insulin sensitivity in T2DM cases in comparison with healthy controls. Induction of inflammation and up regulation of pro-inflammatory cytokines has been purported to play a significant role in pathogenesis of T2DM and study confirms that the positive correlation of TNF-α with T2DM and hence to insulin sensitivity. These can act as early prediction biomarkers in diagnosis and prognosis of human disease i.e Diabetes Mellitus. Further studies are needed to help clinicians manage and treat T2DM effectively.
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Françozo de Melo, Adriana, Giulia Oliveira Timo, and Mauricio Homem-de-Mello. "Vitamin C and Sepsis." In Antioxidants - Benefits, Sources, Mechanisms of Action. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.95623.
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Vitamin C is a supplement used orally by several people globally. It may help in many other conditions, like sepsis, which is caused by an infection that leads to an imbalanced immune response involving pro (e.g., TNF-α, IL-1, IL-2, IL-6) and anti-inflammatory (e.g., IL-10, IL-4, IL-7) cytokines. Ascorbic acid is an antioxidant and acts against reactive oxygen species. At the same time, this vitamin influences cellular immune signaling, avoiding exacerbated transcription of pro-inflammatory cytokines. Very high intravenous doses have already shown to be beneficial in septic patients. Some clinical trials are still running to evaluate the real impact of vitamin C in this condition. To the moment, the combination of low-dose corticosteroids, high-dose parenteral ascorbate, and thiamine seems to be the most effective supportive treatment that could help septic patients recover.
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Zolty, Ronald. "The Role of Neurohormonal Systems, Inflammatory Mediators and Oxydative Stress in Cardiomyopathy." In Cardiomyopathy - Disease of the Heart Muscle. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.97345.
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Cardiomyopathy and more specifically the dilated cardiomyopathy, regardless of severity, is associated with activation of neuro-hormonal, cytokine and oxidative stress signaling pathways that alter the structure and function of cardiac myocytes and non-myocyte cells. These cellular alterations culminate in the morphological changes in cardiac structure termed as cardiac remodeling, a maladaptive process that contributes to further left ventricular dysfunction and heart failure development. This pathological progression is mainly driven by circulating mediators, in particular angiotensin II and norepinephrine. Natriuretic peptides, endothelin-1, vasopressin play also an important role in the progression of the cardiomyopathy. Cardiac inflammation, mediated by cytokines such as tumor necrosis factor-α (TNF-α), interleukins 1 (IL-1) and 6 (IL-6), as well as the oxidative stress were also shown to worsen the cardiac function. Although these pathways have been described separately, they are critically inter-dependent in the response to the development and progression of the dilated cardiomyopathy. This chapter reviews the cellular basis for cardiac remodeling and the mechanisms that contribute to these cellular abnormalities and, more broadly, to the pathophysiology of dilated cardiomyopathy, its progression and its potential treatments.
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Kumar, Vikas, Md Sakhawat Hossain, Janice A. Ragaza, and Marina Rubio Benito. "The Potential Impacts of Soy Protein on Fish Gut Health." In Soybean for Human Consumption and Animal Feed. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.92695.
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Soy protein is the major source of protein as fishmeal replacement in fish feed because of its worldwide availability and low price. However, the presence of high carbohydrate content along with saponins, lectins, and phytates can have a negative impact on fish gut health. Based on the literature and our lab studies, dietary soybean meal can cause a dose-dependent type of distal intestine inflammation called enteritis in commercial fish species including salmonids. This leads to reduced absorptive capacity, increased mucus secretion, hyperpermeability, and leucocyte infiltration in the lamina propria and submucosa, also inducing the pro-inflammatory cytokine genes expression, including Il-1β, Il-8, and Tnf-α. In addition, dietary soy may alter the composition and population of the gut microbiota via providing nutrients and energy that preferentially support the growth of some gut bacteria. This chapter summarizes the current knowledge of the effects of soy protein on the enteritis and gut microbiota.
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Arora, Disha, Sanjay Sharma, and Sumeet Gupta. "Natural Products Targeting Various Mediators in Rheumatoid Arthritis." In Natural Products for the Management of Arthritic Disorders, 135–63. BENTHAM SCIENCE PUBLISHERS, 2022. http://dx.doi.org/10.2174/9789815050776122010009.
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Rheumatoid arthritis (RA) is a chronic autoimmune disease that leads to an inflammatory reaction, primarily affecting synovial joints and progressive cartilage and bone destruction resulting in gradual joint immobility. Possibly, a diversity of pharmacological intercessions are employed for treating arthritis. But modern treatment is linked with serious adverse outcomes and high expenses. Therefore, alternative therapies have been under examination. Scientific facts on RA have revealed that conventional therapy offers a favourable impact by various actions (cellular) like repression of oxidative stress, down-regulation of pro-inflammatory cytokines, such as IL-6, NF-ƙB, and TNF-α, and inhibiting cartilage degradation. A wide range of active phytoconstituents from the medicinal plants, such as terpenes, anthraquinones, glycosylflavons, flavonols, dihydroflavonols, lignans, coumarins, phytoestrogens, sesquiterpene lactones, thymoquinone, and alkaloids reduced the arthritic manifestations through selecting the pro-inflammatory indicators, which play a role in the pathogeny of the disease (RA). With numerous developments in the last few years regarding functional studies or characterization of plant materials, the phase is put down for extensive scientific trials or using the plants or their products to manage rheumatoid arthritis. The chapter discusses the plants used conventionally with phytoconstituents having anti-inflammatory action. This, in turn, leads to the innovation of new benefits from natural products in the future.
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Sahu, Bijayani, Amy R. Mackos, Angela M. Floden, Loren E. Wold, and Colin K. Combs. "Particulate Matter Exposure Exacerbates Amyloid-β Plaque Deposition and Gliosis in APP/PS1 Mice." In Advances in Alzheimer’s Disease. IOS Press, 2021. http://dx.doi.org/10.3233/aiad210013.
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Background: Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by the accumulation of amyloid-β (Aβ) plaques, neuroinflammation, and neuronal death. There are several well-established genetic and environmental factors hypothesized to contribute to AD progression including air pollution. However, the molecular mechanisms by which air pollution exacerbates AD are unclear. Objective: This study explored the effects of particulate matter exposure on AD-related brain changes using the APP/PS1 transgenic model of disease. Methods: Male C57BL/6;C3H wild type and APP/PS1 mice were exposed to either filtered air (FA) or particulate matter sized under 2.5 μm (PM2.5) for 6 h/day, 5 days/week for 3 months and brains were collected. Immunohistochemistry for Aβ, GFAP, Iba1, and CD68 and western blot analysis for PS1, BACE, APP, GFAP, and Iba1 were performed. Aβ ELISAs and cytokine arrays were performed on frozen hippocampal and cortical lysates, respectively. Results: The Aβ plaque load was significantly increased in the hippocampus of PM2.5-exposed APP/PS1 mice compared to their respective FA controls. Additionally, in the PM2.5-exposed APP/PS1 group, increased astrocytosis and microgliosis were observed as indicated by elevated GFAP, Iba1, and CD68 immunoreactivities. PM2.5 exposure also led to an elevation in the levels of PS1 and BACE in APP/PS1 mice. The cytokines TNF-α, IL-6, IL-1β, IFN-γ, and MIP-3α were also elevated in the cortices of PM2.5-exposed APP/PS1 mice compared to FA controls. Conclusion: Our data suggest that chronic particulate matter exposure exacerbates AD by increasing Aβ plaque load, gliosis, and the brain inflammatory status.
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Hu, Li, Shaoping Zhu, Xiaoping Peng, Kanglan Li, Wanjuan Peng, Yu Zhong, Chenyao Kang, Xingxing Cao, Zhou Liu, and Bin Zhao. "High Salt Elicits Brain Inflammation and Cognitive Dysfunction, Accompanied by Alternations in the Gut Microbiota and Decreased SCFA Production." In Advances in Alzheimer’s Disease. IOS Press, 2022. http://dx.doi.org/10.3233/aiad220029.
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Background: Excessive salt intake is considered as an important risk factor for cognitive impairment, which might be the consequence of imbalanced intestinal homeostasis. Objective: To investigate the effects of dietary salt on the gut microbiota and cognitive performance and the underlying mechanisms. Methods: Adult female C57BL/6 mice were maintained on either normal chow (control group, CON) or sodium-rich chow containing 8% NaCl (high-salt diet, HSD) for 8 weeks. Spatial learning and memory ability, short-chain fatty acids (SCFAs) concentrations, gut bacterial flora composition, blood-brain barrier permeability, and proinflammatory cytokine levels and apoptosis in the brain were evaluated. Results: The mice fed a HSD for 8 weeks displayed impaired learning and memory abilities. HSD significantly reduced the proportions of Bacteroidetes (S24-7 and Alloprevotella) and Proteobacteria and increased that of Firmicutes (Lachnospiraceae and Ruminococcaceae). SCFA concentrations decreased in the absolute concentrations of acetate, propionate, and butyrate in the fecal samples from the HSD-fed mice. The HSD induced both BBB dysfunction and microglial activation in the mouse brain, and increased the IL-1β, IL-6, and TNF-α expression levels in the cortex. More importantly, the degree of apoptosis was higher in the cortex and hippocampus region of mice fed the HSD, and this effect was accompanied by significantly higher expression of cleaved caspase-3, caspase-3, and caspase-1. Conclusion: The HSD directly causes cognitive dysfunction in mice by eliciting an inflammatory environment and triggering apoptosis in the brain, and these effects are accompanied by gut dysbiosis, particularly reduced SCFA production.
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Malhotra, Hitesh, Anjoo Kamboj, and Peeyush Kaushik. "Phytochemicals: A New Approach for Targeting Biomarkers in the Management of Arthritis." In Natural Products for the Management of Arthritic Disorders, 218–42. BENTHAM SCIENCE PUBLISHERS, 2022. http://dx.doi.org/10.2174/9789815050776122010013.
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Rheumatoid arthritis (RA) is an autoimmune inflammatory condition that involves the destruction of bone as well as cartilage architecture and induces extensive joint pain, stiffness and swelling. The condition is characterized by the infiltration of inflammatory cytokines, such as IL-1, TNF-α, which results in synovial hyperplasia and pannus formation. Currently, no effective curative treatment is available for RA patients and the existing ones produce numerous unwanted effects. So, phytoconstituents have been considered as a potential source for many such chronic conditions with minimal side effects. Phytomolecules such as Andrographolide, Berberine, Curcumin, Ginsenoside, Hesperidin, Kirenol, Madecassocide and various other polyphenolic compounds are under clinical or pre-clinical trials for their anti.arthritic efficacy. Phytochemicals used in the treatment of arthritis target the inflammatory signaling pathway and hyperactive immune reactions. The compounds, in addition to anti-inflammatory activity, also suppress bone erosion and osteoclastic activity. Furthermore, phytomolecules inhibit the release and generation of reactive oxygen species and proinflammatory cytokines.
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Ali, Anwar, Quratul Ain, Ayesha Saeed, Waseem Khalid, Munir Ahmed, and Ahmed Bostani. "Bio-Molecular Characteristics of Whey Proteins with Relation to Inflammation." In Whey Proteins - Uses and Biological Roles [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.99220.
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Whey proteins in bovine milk are a mixture of globular proteins manufactured from whey which is a byproduct of cheese industry. Whey protein is categorized to contain plethora of healthy components due to wide range of pH, promising nutritional profile with cost effective and diverse functionality. Reportedly there are three categories of whey protein, whey protein concentrate (WPC) (29–89%); whey protein isolate (WPI) 90% and whey protein hydrolysate (WPH) on the basis of proteins present in them. Whey proteins is composed of β-lactoglobulin (45–57%), immunoglobulins (10–15%) α-lactalbumin (15–25%), glicomacropeptide (10–15%), lactoperoxidase (<1%) and lactoferrin nearly (1%). Whey protein plays an important role and is validated to confer anti-inflammatory and immunostimulatory roles related to all metabolic syndromes. According to molecular point of view whey proteins decrease inflammatory cytokines (IL-1α, IL-1β, IL-10 and TNF- α); inhibits ACE and NF-κB expression; promotes Fas signaling and caspase-3 expression; elevates GLP-1, PYY, CCK, G1P and leptin; chelate and binds Fe+3, Mn+3 and Zn+2. In this chapter we will discuss significant biological role of whey proteins related to inflammatory health issues.
Conference papers on the topic "Pro-inflammatory cytokine TNF -α"
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Danilova, Galina, and Anna Klinnikova. "INFLUENCE OF GLUCOCORTICOID HORMONES ON THE INFLAMMATORY EFFECTS OF THE PRO-INFLAMMATORY CYTOKINE TNF-α." In XVIII INTERNATIONAL INTERDISCIPLINARY CONGRESS NEUROSCIENCE FOR MEDICINE AND PSYCHOLOGY. LCC MAKS Press, 2022. http://dx.doi.org/10.29003/m2739.sudak.ns2022-18/120.
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Wolfe, Valerie M., Seonghun Park, Marjana Tomic, Peter A. Torzilli, and C. T. Christopher Chen. "Load Down-Regulates TNF-Alpha Induced Cartilage Degradation in Part Through NF-KB and P38 Pathways." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176541.
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Pro-inflammatory cytokines, such as interleukin-1 (IL-1) and tumor necrosis factor (TNF), can induce cartilage degradation after acute injury or in inflammatory diseases [1,2,3,7]. The degradative events are coordinated through the elevation and activation of two classes of enzymes, namely matrix metalloproteinases (MMPs) and aggrecanases (ADAMTS-4 and −5) [1,6]. Prior studies suggested that pro-inflammatory responses induced by IL-1β can be inhibited by tensile load [2] and more recently by cyclic compression [8]. It is, however, not clear whether load affects other cytokines, such as TNF-α. TNF-α is known to bind its receptor (TNFR1) to cause a cascade that ends with degradation of an inhibitor, IκBα, and release of the transcription factor NF-κB [3]. The actions of TNF-α are also known to be affected by at least three NF-κB independent pathways including the p38, ERK, and JNK pathways [4]. The objective of this study was to determine whether cyclic compression could affect TNF-α induced cartilage degradation and to determine the roles of p38, ERK, and JNK pathways in TNF-induced cartilage degradation. We hypothesized that cyclic loading would inhibit the degradative effects caused by TNF-α.
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Rajan, Neena, Nathaniel Stetson, Passquale Razzano, Mitchell Levine, Daniel Grande, and Nadeen Chahine. "Response of Mesenchymal Stem Cells and Intervertebral Disc Cells to Inflammatory Challenge." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53937.
Full textAbstract:
Human intervertebral disc (IVD) degeneration is accompanied by elevated levels of pro-inflammatory cytokines, particularly IL-1β and TNF-α [1–3]. Cytokine secretion by disc cells increases catabolic breakdown of the tissue, resulting in a positive feedback of disc integrity loss and further inflammation [4–6]. A recent study by our group has shown that severity of degeneration in an injury model can influence the therapeutic effect of cell based repair, such as treatment with mesenchymal stem cells (MSCs) [7]. The goal of this study is to measure the response of MSCs to inflammatory challenge, and to compare this response to that of differentiated disc cells from the nucleus pulposus (NP), annulus fibrosis (AF) and end plate (EP). In this study, we investigated the effects of lipopolysaccharide (LPS) on intervertebral disc cells and MSCs viability, pro-inflammatory cytokine expression and extracellular matrix (ECM) expression. LPS is an endotoxin that induces strong immune responses in animal tissue and hence widely used as a pre-clinical model of inflammation. This approach provides an opportunity to study broad aspects of the physiological inflammatory process observed in degenerative disc disease.
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Maidhof, Robert, Neena Rajan, and Nadeen O. Chahine. "Effect of Inflammation on the Osmotic Response of Nucleus Pulposus Cells." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80358.
Full textAbstract:
Intervertebral disc (IVD) degeneration is accompanied by elevated levels of pro-inflammatory cytokines, particularly IL-1β and TNF-α [1]. Disc cells from the nucleus pulposus (NPs) respond to cytokine stimulation with increased catabolic breakdown of the tissue, resulting in a positive feedback of disc integrity loss and further inflammation [2]. Previous studies by our group have examined the response of NP cells to Toll-Like Receptor-4 (TLR-4) activation through stimulation with lipopolysaccharide (LPS). TLR-4 is a pattern recognition receptor that is activated in innate immunity and by polysaccharide fragments from degenerated proteoglycans. TLR-4 activation by LPS results in stimulation of multiple cytokines by NP cells [3]. Moreover, we have shown that in vivo LPS injection results in catabolic changes in the IVD, including matrix breakdown, decrease in biomechanical properties and loss of disc height [4]. However, the specific cellular mechanisms for these catabolic changes remain to be elucidated.
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Rajan, Neena, Nate Stetson, Robert Maidhof, Mitchell Levine, and Nadeen Chahine. "In Vivo Administration of an Inflammatory Stimulant can Trigger Loss of Biomechanical and Biochemical Properties of the Intervertebral Disc." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80495.
Full textAbstract:
Human intervertebral disc (IVD) degeneration is accompanied by chronic inflammation, particularly seen in the elevated levels of pro-inflammatory cytokines IL-1β and TNF-α [1–3]. Animal models of disc degeneration (DD) using stab or laceration of the disc generally reproduce morphological changes of IVD degeneration. However, inflammatory changes in these models are thought to be acute and transient post injury [4–6]. The goal of this study is to explore the effect of direct inflammatory stimulation of the IVD on disc biochemical and biomechanical properties in vivo. We utilize lipopolysaccharide (LPS), an inflammatory stimulant that provokes secretion of multiple cytokines by disc cells. We have previously shown that direct injection of LPS into the disc results in significantly higher protein levels of IL-1β, TNF-α, HMGB-1 and MIF vs. sham injection up to 7 days post administration [7]. The goal of this study is to explore the dose-dependent response of this inflammatory stimulation on the biochemical and biomechanical properties of IVD in vivo. We hypothesize that LPS stimulation mimics the pathophysiology of DD by triggering a group of cytokines that are associated with IVD degeneration. LPS is administered using micro needles (<10% disc height) in order to minimize the potential disruption by needle injection.
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Danilova, G. А., A. A. Klinnikova, and N. P. Aleksandrova. "The role of prostaglandins in the realization of respiratory effects of TNF-α in case of hypoxia." In VIII Vserossijskaja konferencija s mezhdunarodnym uchastiem «Mediko-fiziologicheskie problemy jekologii cheloveka». Publishing center of Ulyanovsk State University, 2021. http://dx.doi.org/10.34014/mpphe.2021-86-88.
Full textAbstract:
At the present time very little is known about interactions between systemic inflammation and control of respiration. The aim of this study was to compare the respiratory effects of the main inflammatory cytokine TNF - α before and after pretreatment with diclofenac, a nonspecific cyclooxygenase (COX) inhibitor.
In experiments on anesthetized, tracheostomized rats, pneumotachometry method was used to measure peak airflow and respiratory rate. The ventilatory response to hypoxia was investigated by the rebreathing method. It is shown that an increase in the systemic level of TNF – α causes a significant increase in the minute volume of respiration, tidal volume, the average speed of the inspiratory flow. In contrast the slope of the hypoxic ventilatory response decreased after administration of TNF-α. Diclofenac pretreatment eliminated these respiratory effects of TNF - α. The data indicate that the ability of TNF - α to enhance basal ventilation and to reduce the ventilatory hypoxic response is mediated by the cyclooxygenase pathway.
Key words: tumor necrosis factor – α, hypoxia, prostaglandins, peripheral chemoreception, respiration.
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Kashyap, Meghana, Kristen T. Carter, Brent C. Sauer, and Christopher T. Chen. "NF-κB Mediates Cartilage Degradation Induced by Trauma Injury and Interleukin-1." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14513.
Full textAbstract:
Chondrocyte death, induced by impact injury (necrosis) and/or apoptotic inducers such as cytokines, and high level of nitric oxide, is important for the development of post-traumatic arthritis (PTA) [1–3]. The upregulation of pro-inflammatory cytokines, such as interleukin −1 (IL-1) and Tumor necrosis factor (TNF) α, is known to mediate cartilage degradation in inflammatory diseases and after trauma injury [1,2, 6–9]. IL-1 induces the degradation of proteoglycan (PG) in cartilage through NF-κB and Mitogen-activated protein kinases (MAPK: p38, ERK and JNK) pathways [1,2,6]. IL-1 is highly upregulated in synovial joint after impact injury, but the role of IL-1 induced chondrocyte death and matrix/PG degradation in injured cartilage is not completely clear.
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Al-Haidose, Amal. "Effect of Omega-3 Polyunsaturated Fatty Acids on Inflammatory Biomarkers in Chronic Obstructive Pulmonary Disease." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0144.
Full textAbstract:
Chronic obstructive pulmonary disease (COPD) is a chronic progressive inflammatory disease characterised by airflow limitation. Several pro-inflammatory markers are thought to be involved in the pathogenesis of COPD. Cigarette smoking is a major risk factor for COPD, and diet may be a modifiable risk factor for its progression & management. Dietary supplementation with omega3 polyunsaturated fatty acids (omega-3 PUFAs) may be effective therapeutically in patient COPD. Aim: To determine the plasma basal level of inflammatory biomarkers in the study population, to determine the inflammatory biomarkers release from Peripheral blood mononuclear (PBMCs), and to investigate the effect of omega-3 PUFAs, on inflammatory biomarkers released from PBMCs. Methods: Blood samples were collected from 42 subjects; patients with COPD, 15 healthy smokers (HS), and 12 healthy groups (HNS). Selected biomarkers level was measured in Plasma and PBMCs by ELISA. Individual lipid profile analysis was carried out on RBCs fraction. Result: Plasma high levels of CRP and Fibrinogen and low level of CC-16 were observed in COPD patients when compared with healthy controls. The basal release of IL6, IL8, TNFα, and CD31 from PBMCs was significantly differing in COPD and HS groups compared to HNS group. Omega-3 PUFA (EPA and DHA) reduce IL-6, IL-8 and TNF-α release from PBMCs. The fatty acid composition of the erythrocyte membranes in patients group was unmodified. Discussion: This study showed that high level of several inflammatory biomarkers that were detected systemically in COPD group might associate with the disease systemic inflammation. EPA and DHA possess the ability to reduce the cytokines production from COPD inflammatory immune cells. Additionally, no correlation was observed between fatty acid profile analysis and COPD.
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Na Takuathung, M., A. Wongnoppavich, A. Panthong, P. Khonsung, N. Chiranthanut, N. Soonthornchareonnon, and S. Sireeratawong. "Anti-psoriatic Effects of Wannachawee Recipe on TNF-α- and IFN-γ-Induced Inflammatory Cytokine production in HaCaT Human Keratinocytes." In GA 2017 – Book of Abstracts. Georg Thieme Verlag KG, 2017. http://dx.doi.org/10.1055/s-0037-1608165.
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"Pro-inflammatory cytokines “Tumor necrosis factor alpha (TNF-α) and Interleukin beta (IL-1 β)” levels in albino rats after co-administration of diclofenac sodium and dexamethasone." In 2nd Hawler Pharmaceutical Sciences Conference. Hawler Medical University, 2020. http://dx.doi.org/10.15218/hpsc.02.13.
Full textReports on the topic "Pro-inflammatory cytokine TNF -α"
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Cao, Xianling, Xuanyou Zhou, Naixin Xu, Songchang Chang, and Chenming Xu. Association of IL-4 and IL-10 Polymorphisms with Preterm Birth Susceptibility: A Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, April 2022. http://dx.doi.org/10.37766/inplasy2022.4.0044.
Full textAbstract:
Review question / Objective: The aim of our systematic review and meta-analysis was to summarize the effects of IL-4 and IL-10 gene polymorphism and clarify their possible association with PTB. Condition being studied: World Health Organization (WHO) defines preterm birth (PTB) as babies born alive before 37 weeks of pregnancy are completed. The new estimates show that the prevalence of PTB during 2014 ranged from 8.7% to13.4% of all live births, about 15 million preterm babies born each year. Besides, PTB is the leading cause of death worldwide for children below 5 years of age. Babies born preterm are at an increased risk of short-term and long-term complications attributed to immaturity of multiple organ systems, such as cerebral palsy, intellectual disabilities, vision and hearing impairments, and impaired cognitive development. PTB has become a worldwide public health problem, but its etiology remains unclear. Accumulating evidence shows that PTB is a syndrome that can be attributed to a variety of pathological processes(5). Inflammatory diseases and genetic background are known risk factors for PTB, many studies had shown that genetic variations in proinflammatory cytokines such as tumor necrosis factor-α (TNF-α) and interleukin-1 α (IL-1 α) are associated with increased risk of PTB, but the relationship between genetic polymorphism in anti-inflammatory cytokines and risk of PTB remains controversial.
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Schwartz, Bertha, Vaclav Vetvicka, Ofer Danai, and Yitzhak Hadar. Increasing the value of mushrooms as functional foods: induction of alpha and beta glucan content via novel cultivation methods. United States Department of Agriculture, January 2015. http://dx.doi.org/10.32747/2015.7600033.bard.
Full textAbstract:
During the granting period, we performed the following projects: Firstly, we differentially measured glucan content in several pleurotus mushroom strains. Mushroom polysaccharides are edible polymers that have numerous reported biological functions; the most common effects are attributed to β-glucans. In recent years, it became apparent that the less abundant α-glucans also possess potent effects in various health conditions. In our first study, we explored several Pleurotus species for their total, β and α-glucan content. Pleurotuseryngii was found to have the highest total glucan concentrations and the highest α-glucans proportion. We also found that the stalks (stipe) of the fruit body contained higher glucan content then the caps (pileus). Since mushrooms respond markedly to changes in environmental and growth conditions, we developed cultivation methods aiming to increase the levels of α and β-glucans. Using olive mill solid waste (OMSW) from three-phase olive mills in the cultivation substrate. We were able to enrich the levels mainly of α-glucans. Maximal total glucan concentrations were enhanced up to twice when the growth substrate contained 80% of OMSW compared to no OMSW. Taking together this study demonstrate that Pleurotuseryngii can serve as a potential rich source of glucans for nutritional and medicinal applications and that glucan content in mushroom fruiting bodies can be further enriched by applying OMSW into the cultivation substrate. We then compared the immune-modulating activity of glucans extracted from P. ostreatus and P. eryngii on phagocytosis of peripheral blood neutrophils, and superoxide release from HL-60 cells. The results suggest that the anti-inflammatory properties of these glucans are partially mediated through modulation of neutrophileffector functions (P. eryngiiwas more effective). Additionally, both glucans dose-dependently competed for the anti-Dectin-1 and anti-CR3 antibody binding. We then tested the putative anti-inflammatory effects of the extracted glucans in inflammatory bowel disease (IBD) using the dextran sulfate sodium (DSS)–induced model in mice. The clinical symptoms of IBD were efficiently relieved by the treatment with two different doses of the glucan from both fungi. Glucan fractions, from either P. ostreatus or P. eryngii, markedly prevented TNF-α mediated inflammation in the DSS–induced inflamed intestine. These results suggest that there are variations in glucan preparations from different fungi in their anti-inflammatory ability. In our next study, we tested the effect of glucans on lipopolysaccharide (LPS)-induced production of TNF-α. We demonstrated that glucan extracts are more effective than mill mushroom preparations. Additionally, the effectiveness of stalk-derived glucans were slightly more pronounced than of caps. Cap and stalk glucans from mill or isolated glucan competed dose-dependently with anti-Dectin-and anti-CR-3 antibodies, indicating that they contain β-glucans recognized by these receptors. Using the dextran sulfate sodium (DSS)-inflammatory bowel disease mice model, intestinal inflammatory response to the mill preparations was measured and compared to extracted glucan fractions from caps and stalks. We found that mill and glucan extracts were very effective in downregulatingIFN-γ and MIP-2 levels and that stalk-derived preparations were more effective than from caps. The tested glucans were equally effective in regulating the number of CD14/CD16 monocytes and upregulating the levels of fecal-released IgA to almost normal levels. In conclusion, the most effective glucans in ameliorating some IBD-inflammatory associated symptoms induced by DSS treatment in mice were glucan extracts prepared from the stalk of P. eryngii. These spatial distinctions may be helpful in selecting more effective specific anti-inflammatory mushrooms-derived glucans. We additionally tested the effect of glucans on lipopolysaccharide-induced production of TNF-α, which demonstrated stalk-derived glucans were more effective than of caps-derived glucans. Isolated glucans competed with anti-Dectin-1 and anti-CR3 antibodies, indicating that they contain β-glucans recognized by these receptors. In conclusion, the most effective glucans in ameliorating IBD-associated symptoms induced by DSS treatment in mice were glucan extracts prepared from the stalk of P. eryngii grown at higher concentrations of OMSW. We conclude that these stress-induced growing conditions may be helpful in selecting more effective glucans derived from edible mushrooms. Based on the findings that we could enhance glucan content in Pleurotuseryngii following cultivation of the mushrooms on a substrate containing different concentrations of olive mill solid waste (OMSW) and that these changes are directly related to the content of OMSW in the growing substrate we tested the extracted glucans in several models. Using dextran sulfate sodium (DSS)–inflammatory bowel disease (IBD) mice model, we measured the colonic inflammatory response to the different glucan preparations. We found that the histology damaging score (HDS) resulting from DSS treatment reach a value of 11.8 ± 2.3 were efficiently downregulated by treatment with the fungal extracted glucans, glucans extracted from stalks cultivated at 20% OMSWdownregulated to a HDS value of 6.4 ± 0.5 and at 80% OMSW showed the strongest effects (5.5 ± 0.6). Similar downregulatory effects were obtained for expression of various intestinal cytokines. All tested glucans were equally effective in regulating the number of CD14/CD16 monocytes from 18.2 ± 2.7 % for DSS to 6.4 ± 2.0 for DSS +glucans extracted from stalks cultivated at 50% OMSW. We finally tested glucans extracted from Pleurotuseryngii grown on a substrate containing increasing concentrations of olive mill solid waste (OMSW) contain greater glucan concentrations as a function of OMSW content. Treatment of rat Intestinal epithelial cells (IEC-6) transiently transfected with Nf-κB fused to luciferase demonstrated that glucans extracted from P. eryngii stalks grown on 80% OMSWdownregulatedTNF-α activation. Glucans from mushrooms grown on 80% OMSW exerted the most significant reducing activity of nitric oxide production in lipopolysaccharide (LPS) treated J774A.1 murine macrophages. The isolated glucans were tested in vivo using the Dextran Sodium Sulfate (DSS) induced colitis in C57Bl/6 mice and found to reduce the histology damaging score resulting from DSS treatment. Expression of various intestinal cytokines were efficiently downregulated by treatment with the fungal extracted glucans. We conclude that the stress-induced growing conditions exerted by OMSW induces production of more effective anti-inflammatory glucans in P. eryngii stalks.