Journal articles on the topic 'Pro-inflammatory cytokine TNF -α'
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1
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.
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Trenova, Anastasiya G., Mariya G. Manova, Ivanka I. Kostadinova, Mariana A. Murdjeva, Dimka R. Hristova, Tonka V. Vasileva, and Zahari I. Zahariev. "Clinical and laboratory study of pro-inflammatory and anti-inflammatory cytokines in women with multiple sclerosis." Folia Medica 53, no. 2 (June 1, 2011): 29–35. http://dx.doi.org/10.2478/v10153-010-0034-x.
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Abstract Multiple sclerosis (MS) is an autoimmune demyelinating disorder of the central nervous system characterised with a complex system of interactions between proinflammatory and anti-inflammatory cytokines in its course. Aim: The aim of the present study was to investigate the serum levels of cytokines TNF-α, IFN- γ, IL- 4 and IL- 10 in female patients with MS and healthy individuals, the changes occurring in the relapse and remission phases of the disease and their correlation with the severity of the neurological deficit. Patients and methods: Thirty-five women with relapsing-remitting MS were examined. The patients’ age ranged between 18 and 50 years and MS was verified clinically and by magnetic resonance imaging according to the McDonald criteria. Thirteen of the patients were treated with interferon-β-1b. The serum concentrations of TNF-α, IFN- γ, IL- 4 and IL- 10 were determined twice - in relapse and in remission - using an enzyme-linked immunosorbent assay (EL ISA). The control group consisted of 35 age-matched healthy females. Results: The comparison of cytokine serum concentrations during the two phases of the disease showed significant elevation of the TNF-α serum levels in the relapse phase and of IL- 4 - in the remission phase. The comparison between the patients and the healthy control subjects demonstrated statistically significant lower concentrations of TNF-α in remission patients and higher concentrations of IL- 10 in relapse patients. The patients with interferon-β-1b treatment showed different profile of cytokine secretion from the patients without interferon-β-1b treatment. Interferon-β-1b-treated patients showed significantly lower serum levels of TNF-α and IFN- γ during the relapse phase and higher TNF-α and IL- 10 serum levels during the remission phase compared with the untreated patients. Conclusions: Serum levels of TNF-α and IL- 4 objectively reflect the immune response during relapse and remission of the disease. The severity of neurological deficit as estimated with the expanded disability status scale (EDSS ) does not depend on the serum levels of TNF-α, IL- 10 and IFN- γ in the two phases of MS.
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Habil, N., W. Abate, J. Beal, and A. D. Foey. "Heat-killed probiotic bacteria differentially regulate colonic epithelial cell production of human β-defensin-2: dependence on inflammatory cytokines." Beneficial Microbes 5, no. 4 (December 1, 2014): 483–95. http://dx.doi.org/10.3920/bm2013.0061.
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The inducible antimicrobial peptide human β-defensin-2 (hBD-2) stimulated by pro-inflammatory cytokines and bacterial products is essential to antipathogen responses of gut epithelial cells. Commensal and probiotic bacteria can augment such mucosal defences. Probiotic use in the treatment of inflammatory bowel disease, however, may have adverse effects, boosting inflammatory responses. The aim of this investigation was to determine the effect of selected probiotic strains on hBD-2 production by epithelial cells induced by pathologically relevant pro-inflammatory cytokines and the role of cytokine modulators in controlling hBD-2. Caco-2 colonic intestinal epithelial cells were pre-incubated with heat-killed probiotics, i.e. Lactobacillus casei strain Shirota (LcS) or Lactobacillus fermentum strain MS15 (LF), followed by stimulation of hBD-2 by interleukin (IL)-1β and tumour necrosis factor alpha (TNF-α) in the absence or presence of exogenous IL-10 or anti-IL-10 neutralising antibody. Cytokines and hBD-2 mRNA and protein were analysed by real-time quantitative polymerase chain reaction and enzyme-linked immunosorbent assay. LcS augmented IL-1β-induced hBD-2, whereas LF enhanced TNF-α- and suppressed IL-1β-induced hBD-2. LF enhanced TNF-α-induced TNF-α and suppressed IL-10, whereas augmented IL-1β-induced IL-10. LcS upregulated IL-1β-induced TNF-α mRNA and suppressed IL-10. Endogenous IL-10 differentially regulated hBD-2; neutralisation of IL-10 augmented TNF-α- and suppressed IL-1β-induced hBD-2. Exogenous IL-10, however, suppressed both TNF-α- and IL-1β-induced hBD-2; LcS partially rescued suppression in TNF-α- and IL-1β-stimulation, whereas LF further suppressed IL-1β-induced hBD-2. It can be concluded that probiotic strains differentially regulate hBD-2 mRNA expression and protein secretion, modulation being dictated by inflammatory stimulus and resulting cytokine environment.
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Kim, Seon-Young, Jae-Min Kim, Sung-Wan Kim, Il-Seon Shin, Min-Ho Park, Jung-Han Yoon, Chan Choi, and Jin-Sang Yoon. "Associations between Plasma Cytokines and Depressive Mood in Patients with Breast Cancer." International Journal of Psychiatry in Medicine 43, no. 1 (January 2012): 1–17. http://dx.doi.org/10.2190/pm.43.1.a.
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Objective: The few studies on the associations between cytokines and depressive mood in patients with cancer have produced conflicting results. This study investigated the associations between plasma cytokines and depressive mood in patients with breast cancer using a large panel of pro-inflammatory, anti-inflammatory, and immune-modulating cytokines. Methods: We recruited 273 hospitalized patients with breast cancer awaiting surgery. Preoperative plasma samples were obtained for cytokine analysis, including pro-inflammatory (interleukin [IL]-2, IL-12, interferon [IFN]-γ, and tumor necrosis factor [TNF-α]), anti-inflammatory (IL-4, IL-5, IL-10, and IL-13), and immune-modulating (granulocyte/macrophage colony-stimulating factor [GM-CSF]) cytokines. Depressive mood was measured using the Montgomery—Asberg Depression Rating Scale (MADRS) at 2–5 days postoperatively, when the patients could cooperate. Covariates included various demographic and clinical characteristics. The association between the MADRS score and each cytokine level was estimated using linear regression models. Results: Cytokine levels were significantly inter-correlated. Depressive mood was associated with lower levels of pro-inflammatory (IL-2, IL-12, and TNF-α), anti-inflammatory (IL-5, IL-10, and IL-13), and immune-modulating (GM-CSF) cytokines independent of potential covariates such as living area or functional level. Conclusions: The findings suggest that depressive mood is associated with a generally decreased inflammatory reaction or immune function in patients with breast cancer.
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Parra-Izquierdo, Iván, Tania Sánchez-Bayuela, Javier López, Cristina Gómez, Enrique Pérez-Riesgo, J. Alberto San Román, Mariano Sánchez Crespo, Magdi Yacoub, Adrian H. Chester, and Carmen García-Rodríguez. "Interferons Are Pro-Inflammatory Cytokines in Sheared-Stressed Human Aortic Valve Endothelial Cells." International Journal of Molecular Sciences 22, no. 19 (September 30, 2021): 10605. http://dx.doi.org/10.3390/ijms221910605.
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Calcific aortic valve disease (CAVD) is an athero-inflammatory process. Growing evidence supports the inflammation-driven calcification model, mediated by cytokines such as interferons (IFNs) and tumor necrosis factor (TNF)-α. Our goal was investigating IFNs’ effects in human aortic valve endothelial cells (VEC) and the potential differences between aortic (aVEC) and ventricular (vVEC) side cells. The endothelial phenotype was analyzed by Western blot, qPCR, ELISA, monocyte adhesion, and migration assays. In mixed VEC populations, IFNs promoted the activation of signal transducers and activators of transcription-1 and nuclear factor-κB, and the subsequent up-regulation of pro-inflammatory molecules. Side-specific VEC were activated with IFN-γ and TNF-α in an orbital shaker flow system. TNF-α, but not IFN-γ, induced hypoxia-inducible factor (HIF)-1α stabilization or endothelial nitric oxide synthase downregulation. Additionally, IFN-γ inhibited TNF-α–induced migration of aVEC. Also, IFN-γ triggered cytokine secretion and adhesion molecule expression in aVEC and vVEC. Finally, aVEC were more prone to cytokine-mediated monocyte adhesion under multiaxial flow conditions as compared with uniaxial flow. In conclusion, IFNs promote inflammation and reduce TNF-α–mediated migration in human VEC. Moreover, monocyte adhesion was higher in inflamed aVEC sheared under multiaxial flow, which may be relevant to understanding the initial stages of CAVD.
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Lim, Mei Xing, Huipeng Jiao, Chin Wen Png, Shyong Wei Kevin Tan, and Yongliang Zhang. "Differential regulation of pro-inflammatory cytokine expression by MAP kinases in macrophages in response to intestinal parasite infection (MPF3P.816)." Journal of Immunology 192, no. 1_Supplement (May 1, 2014): 132.16. http://dx.doi.org/10.4049/jimmunol.192.supp.132.16.
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Abstract Blastocystis is a common enteric parasite that is associated with inflammatory bowel disease. However, the pathogenic status of Blastocystis remains unclear. In this study, we found that Blastocystis induced expression of pro-inflammatory cytokines including IL-1β, IL-6 and TNF-α in murine colon and macrophages. We showed that Blastocystis also induced the activation of the three major groups of MAP kinases (ERK, JNK, and p38) in macrophages. The use of MAPK-specific inhibitors in this study demonstrated differential regulation of pro-inflammatory cytokines in macrophages by MAPKs in response to Blastocystis. We found that ERK activation is important for the expression IL-6 and TNF-α at both mRNA and protein levels and the mRNA expression of IL-1β in response to Blastocystis stimulation. Inhibition of JNK significantly suppressed all three pro-inflammatory cytokines at both mRNA and protein levels. p38 inhibition only suppressed IL-6 secretion but not IL-1β and TNF-α. Furthermore, we found that serine proteases from Blastocystis are important for the activation of MAPKs and cytokine expression in macrophages. Our study demonstrated for the first time that Blastocystis could induce the expression of various pro-inflammatory cytokines via activation of MAP kinases, and infection with Blastocystis may contribute to the pathogenesis of inflammatory intestinal diseases through the activation of inflammatory pathways in host immune cells such as macrophages.
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Yamauchi, Nobuhiro, Emika Minagawa, Kazutaka Imai, Kenjiro Kobuchi, Runbo Li, Yoichiro Taguchi, and Makoto Umeda. "High-Intensity Red Light-Emitting Diode Irradiation Suppresses the Inflammatory Response of Human Periodontal Ligament Stem Cells by Promoting Intracellular ATP Synthesis." Life 12, no. 5 (May 15, 2022): 736. http://dx.doi.org/10.3390/life12050736.
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Periodontitis is an inflammatory lesion in the periodontal tissue. The behavior of human periodontal ligament stem cells (hPDLSCs), which play an important role in periodontal tissue regeneration, is restricted by the influence of inflammatory mediators. Photobiomodulation therapy exerts anti-inflammatory effects. The purpose of this study was to investigate the effects of light-emitting diode (LED) irradiation on the inflammatory responses of hPDLSCs. The light source was a red LED (peak wavelength: 650 nm), and the total absolute irradiance was 400 mW/cm2. The inflammatory response in hPDLSCs is induced by tumor necrosis factor (TNF)-α. Adenosine triphosphate (ATP) levels and pro-inflammatory cytokine (interleukin [IL]-6 and IL-8) production were measured 24 h after LED irradiation, and the effects of potassium cyanide (KCN) were investigated. LED irradiation at 6 J/cm2 significantly increased the ATP levels and reduced TNF-α-induced IL-6 and IL-8 production. Furthermore, the inhibitory effect of LED irradiation on the production of pro-inflammatory cytokines was inhibited by KCN treatment. The results of this study showed that high-intensity red LED irradiation suppressed the TNF-α-stimulated pro-inflammatory cytokine production in hPDLSCs by promoting ATP synthesis. These results suggest that high-intensity red LED is a useful tool for periodontal tissue regeneration in chronically inflamed tissues.
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Morceau, F., M. Dicato, and M. Diederich. "Pro-Inflammatory Cytokine-Mediated Anemia: Regarding Molecular Mechanisms of Erythropoiesis." Mediators of Inflammation 2009 (2009): 1–11. http://dx.doi.org/10.1155/2009/405016.
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Anemia of cancer and chronic inflammatory diseases is a frequent complication affecting quality of life. For cancer patients it represents a particularly bad prognostic. Low level of erythropoietin is considered as one of the causes of anemia in these pathologies. The deficiency in erythropoietin production results from pro-inflammatory cytokines effect. However, few data is available concerning molecular mechanisms involved in cytokine-mediated anemia. Some recent publications have demonstrated the direct effect of pro-inflammatory cytokines on cell differentiation towards erythroid pathway, without erythropoietin defect. This suggested that pro-inflammatory cytokine-mediated signaling pathways affect erythropoietin activity. They could interfere with erythropoietin-mediated signaling pathways, inducing early apoptosis and perturbing the expression and regulation of specific transcription factors involved in the control of erythroid differentiation. In this review we summarize the effect of tumor necrosis factor (TNF)α, TNF-related apoptosis-inducing ligand (TRAIL), and interferon (IFN)-γon erythropoiesis with a particular interest for molecular feature.
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Romanowska-Próchnicka, Katarzyna, Anna Felis-Giemza, Marzena Olesińska, Piotr Wojdasiewicz, Agnieszka Paradowska-Gorycka, and Dariusz Szukiewicz. "The Role of TNF-α and Anti-TNF-α Agents during Preconception, Pregnancy, and Breastfeeding." International Journal of Molecular Sciences 22, no. 6 (March 13, 2021): 2922. http://dx.doi.org/10.3390/ijms22062922.
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Tumor necrosis factor-alpha (TNF-α) is a multifunctional Th1 cytokine and one of the most important inflammatory cytokines. In pregnancy, TNF-α influences hormone synthesis, placental architecture, and embryonic development. It was also shown that increased levels of TNF-α are associated with pregnancy loss and preeclampsia. Increased TNF-α levels in complicated pregnancy draw attention to trophoblast biology, especially migratory activity, syncytialisation, and endocrine function. Additionally, elevated TNF-α levels may affect the maternal-fetal relationship by altering the secretory profile of placental immunomodulatory factors, which in turn affects maternal immune cells. There is growing evidence that metabolic/pro-inflammatory cytokines can program early placental functions and growth in the first trimester of pregnancy. Furthermore, early pregnancy placenta has a direct impact on fetal development and maternal immune system diseases that release inflammatory (e.g., TNF-α) and immunomodulatory factors, such as chronic inflammatory rheumatic, gastroenterological, or dermatological diseases, and may result in an abnormal release of cytokines and chemokines in syncytiotrophoblasts. Pregnancy poses a challenge in the treatment of chronic disease in patients who plan to have children. The activity of the disease, the impact of pregnancy on the course of the disease, and the safety of pharmacotherapy, including anti-rheumatic agents, in pregnancy should be considered.
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Hohnstein, Florian S., Marita Meurer, Nicole de Buhr, Maren von Köckritz-Blickwede, Christoph G. Baums, Gottfried Alber, and Nicole Schütze. "Analysis of Porcine Pro- and Anti-Inflammatory Cytokine Induction by S. suis In Vivo and In Vitro." Pathogens 9, no. 1 (January 3, 2020): 40. http://dx.doi.org/10.3390/pathogens9010040.
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Weaning piglets are susceptible to the invasive Streptococcus (S.) suis infection, which can result in septicemia. The aim of this study was to investigate the cytokine profile induced upon S. suis infection of blood, to determine the cellular sources of those cytokines, and to study the potential effects of the induced cytokines on bacterial killing. We measured TNF-α, IL-6, IFN-γ, IL-17A and IL-10 after an experimental intravenous infection with S. suis serotype 2 in vivo, and analyzed whole blood, peripheral blood mononuclear cells (PBMC) and separated leukocytes to identify the cytokine-producing cell type(s). In addition, we used a reconstituted whole blood assay to investigate the effect of TNF-α on bacterial killing in the presence of different S. suis-specific IgG levels. An increase in IL-6 and IL-10, but not in IFN-γ or IL-17A, was observed in two of three piglets with pronounced bacteremia 16 to 20 h after infection, but not in piglets with controlled bacteremia. Our results confirmed previous findings that S. suis induces TNF-α and IL-6 and could demonstrate that TNF-α is produced by monocytes in vitro. We further found that IL-10 induction resulted in reduced secretion of TNF-α and IL-6. Rapid induction of TNF-α was, however, not crucial for in vitro bacterial killing, not even in the absence of specific IgG.
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Arjadi, Fitranto, Sindhu Wisesa, Nor Sri Inayani, Prasetyo Tri Kuncoro, and Catharina Widiartini. "Levels of Cortisol and Inflammatory Cytokines after The Induction of Various Sleep Deprivation Stress Models in Male Wistar Rats." Molekul 17, no. 3 (November 19, 2022): 383. http://dx.doi.org/10.20884/1.jm.2022.17.3.6218.
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Sleep deprivation (SD) can modulate the production of various cytokines, including pro-inflammatory cytokines such as IL-6, TNF-α, and IFN-γ, and anti-inflammatory cytokines such as IL-10. Paradoxical sleep deprivation (PSD) increases the risk of inflammation but can be relieved by sleep recovery (SR). This study aimed to determine the differences in levels of cortisol and inflammatory cytokines (IL-6, IL-10, TNF-α, dan IFN-γ) in male Wistar rats (Rattus norvegicus) after induction of various sleep deprivation stress models. Twenty-five of male Wistar rats were randomly divided into five groups: control, PSD (20 hours of SD/day for five days), Total Sleep Deprivation or TSD (24 hours of SD/day for five days), PSD+SR (PSD followed by SR), and TSD+SR (TSD followed by SR). The plasma cortisol levels were measured with ELISA, and inflammatory cytokine levels were measured with immunoassay and calculated with fold change. Mean cortisol levels were significantly increased in treatment groups compared to the control group (p=0.029). Multivariate analysis showed no statistically significant difference in inflammatory cytokine levels of IL-6 (p=0.658), IL-10 (p=0.065), TNF-α (p=0.399), and IFN-γ (p=0.283) in all groups. In conclusion, various sleep deprivation stress models affect cortisol levels but not inflammatory cytokine levels of IL-6, IL-10, TNF-α, and IFN-γ among male Wistar rats.
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Subedi, Lalita, Si Eun Lee, Syeda Madiha, Bhakta Prasad Gaire, Mirim Jin, Silvia Yumnam, and Sun Yeou Kim. "Phytochemicals against TNFα-Mediated Neuroinflammatory Diseases." International Journal of Molecular Sciences 21, no. 3 (January 24, 2020): 764. http://dx.doi.org/10.3390/ijms21030764.
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Tumor necrosis factor-alpha (TNF-α) is a well-known pro-inflammatory cytokine responsible for the modulation of the immune system. TNF-α plays a critical role in almost every type of inflammatory disorder, including central nervous system (CNS) diseases. Although TNF-α is a well-studied component of inflammatory responses, its functioning in diverse cell types is still unclear. TNF-α functions through its two main receptors: tumor necrosis factor receptor 1 and 2 (TNFR1, TNFR2), also known as p55 and p75, respectively. Normally, the functions of soluble TNF-α-induced TNFR1 activation are reported to be pro-inflammatory and apoptotic. While TNF-α mediated TNFR2 activation has a dual role. Several synthetic drugs used as inhibitors of TNF-α for diverse inflammatory diseases possess serious adverse effects, which make patients and researchers turn their focus toward natural medicines, phytochemicals in particular. Phytochemicals targeting TNF-α can significantly improve disease conditions involving TNF-α with fewer side effects. Here, we reviewed known TNF-α inhibitors, as well as lately studied phytochemicals, with a role in inhibiting TNF-α itself, and TNF-α-mediated signaling in inflammatory diseases focusing mainly on CNS disorders.
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Wagner, Elizabeth M. "TNF-α induced bronchial vasoconstriction." American Journal of Physiology-Heart and Circulatory Physiology 279, no. 3 (September 1, 2000): H946—H951. http://dx.doi.org/10.1152/ajpheart.2000.279.3.h946.
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The pro-inflammatory characteristics of tumor necrosis factor-α (TNF-α) have been extensively characterized in in vitro systems. Furthermore, this cytokine has been shown to play a pivotal role in airways inflammation in asthma. Since the airway vasculature also performs an essential function in inflammatory cell transit to the airways, experiments were performed to determine the effects of TNF-α on bronchial vascular resistance (BVR). In anesthetized, ventilated sheep, the bronchial artery (BA) was cannulated and perfused with autologous blood. BVR was defined as inflow pressure/flow and averaged 6.3 ± 0.2 mmHg · ml−1 · min−1 (±SE) for the 25 sheep studied. Recombinant human TNF-α (10 μg for 20 or 40 min) infused directly into the BA resulted in a significant decrease in BVR to 87% of baseline ( P < 0.05). This vasodilation was followed by a reversal of tone by 120 min and a sustained increase in BVR to 126% of baseline ( P < 0.05). Since others have shown TNF-α caused coronary vasoconstriction through endothelial release of endothelin-1 (ET-1), an ET-1 antagonist was used to block bronchial vasoconstriction. BQ-123, a selective ETA receptor antagonist, was delivered to the bronchial vasculature prior to TNF-α challenge. Attenuation of bronchial vasoconstriction was observed at 120 min ( P < 0.03). Thus TNF-α causes bronchial vasoconstriction by the secondary release of ET-1. Although TNF-α exerts pro-inflammatory actions on most cells of the airways, vasoactive properties of this cytokine likely further contribute to the inflammatory status of the airways.
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Ghosh, Somenath. "Role of Different Hormones (Testosterone, Estrogen, Melatonin, Glucocorticoid, Thyroxin) in Immune Modulation of Thymocyte and Splenocyte Functions of Indian Goat C. hircus: An in vitro Study." Scholars Academic Journal of Pharmacy 10, no. 7 (July 12, 2021): 115–27. http://dx.doi.org/10.36347/sajp.2021.v10i07.002.
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The immune system is coordinated by a number of cytokines which are regarded as chemical messengers of immunity. Some of them are pro-inflammatory (e.g. IL-2), some are anti-inflammatory (e.g. IL-6), some can be regarded as a switch between pro and anti-inflammatory processes (e.g. TNF-α). Further, immune regulation in body is a proper balance between mitosis and apoptosis occurring simultaneously in the body. In the present chapter we explored the spleen and thymus functions by assessing %SR and % apoptotic rate of splenocytes and thymocytes being significantly high levels of cell proliferation (in terms of %SR) and apoptosis rate during monsoon and winter seasons. We noted IL-2 (a pro-inflammatory cytokine), IL-6 (an anti-inflammatory cykine), TNF-α (a switch between pro and anti-inflammatory cytokine) and IFN-γ (a marker of viral infection) in circulation of goats. We noted significantly high levels of IL-2 and TNF-α levels during monsoon and winter but IFN-γ and IL-6 levels were only high during monsoon. Hence, to ameliorate the elevated inflammatory stress level particularly during monsoon goats have evolved a number of adaptive strategies. But, simultaneously during monsoon the gonadal steroid levels are also high which are reported as immune suppressor. Thus, the basic query may arise how goats are proved to be a better survivor under the season of stress (particularly during monsoon) when the level of potent immune enhancer neurohormone melatonin level is also low.
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Llamas Moya, S., L. Boyle, P. B. Lynch, and S. Arkins. "Pro-inflammatory cytokine and acute phase protein responses to low-dose lipopolysaccharide (LPS) challenge in pigs." Animal Science 82, no. 4 (August 2006): 527–34. http://dx.doi.org/10.1079/asc200665.
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AbstractThe objective of this study was to establish the pro-inflammatory cytokine and acute phase protein responses to low-dose lipopolysaccharide (LPS) challenge in pigs and to determine whether these immune parameters could also be measured in saliva. Possible gender differences in the acute phase reaction were also assessed. At 6 weeks of age, 24 male and 24 female pigs were injected intraperitoneally with a single dose of 0 or 5 μg/kg live weight (LW) of LPS fromEscherichia coli(treatment). Matched saliva and blood samples were taken at 0, 2, 4, 8, 12 or 24 h after treatment administration. Samples were analysed for concentrations of the pro-inflammatory cytokines tumor necrosis factor-alpha (TNF-α) and interleukin-1beta (IL-1β), the acute phase proteins C-reactive protein (CRP), serum amyloid A (SAA), haptoglobin (Hp), and cortisol. Low-dose LPS administration increased plasma levels of TNF-α (P<0·001), CRP (P<0·05) and SAA (P<0·05) but did not affect plasma concentrations of IL-1β or Hp (P>0·1). Treatment by time interactions showed that plasma levels of TNF-α and CRP in LPS-treated pigs peaked at 2 h (P<0·001) and 12 h (P<0·01), respectively. Low-dose LPS injection tended to increase plasma concentrations of cortisol (P=0·056) and the response to LPS differed between genders (P<0·05), with females showing higher cortisol responsiveness to the challenge (P<0·01). Males showed higher levels of both cytokines regardless of the treatment (P<0·05), probably due to the inhibition of cytokine synthesis by cortisol. Concentrations of both pro-inflammatory cytokines were consistently detectable in saliva and were present in higher concentrations than in plasma (P<0·001). Hence, plasma TNF-α, CRP and SAA are useful indicators of sub-acute inflammation/infection in pigs as simulated by a low-dose LPS challenge and gender differences exist in the pro-inflammatory cytokine response after a low dose of LPS.
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Iwadou, H., Y. Morimoto, H. Iwagaki, S. Sinoura, Y. Chouda, M. Kodama, T. Yoshioka, S. Saito, T. Yagi, and N. Tanaka. "Differential Cytokine Response in Host Defence Mechanisms Triggered by Gram-Negative and Gram-Positive Bacteria, and the Roles of Gabexate Mesilate, a Synthetic Protease Inhibitor." Journal of International Medical Research 30, no. 2 (April 2002): 99–108. http://dx.doi.org/10.1177/147323000203000201.
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Bacterial infection results in the production of inflammatory mediators and may be involved in the pathogenesis of sepsis and/or systemic inflammatory response syndrome. The effect of lipopolysaccharide (LPS), a major component of the outer surface of Gram-negative bacteria, and Staphylococcal enterotoxin B (SEB), a superantigen of Gram-positive bacteria, on cytokine production in peripheral blood mononuclear cells (PBMCs) was examined. LPS significantly increased the production of proinflammatory and anti-inflammatory cytokines, and SEB enhanced the production of helper T lymphocyte type cytokines. These results illustrated the different responses to Gram-negative and Gram-positive bacterial infections. The effect of gabexate mesilate, a synthetic protease inhibitor, on cytokine production and expression of the toll-like receptor (TLR) was also examined. The results suggest that gabexate mesilate-induced inhibition of tumour necrosis factor-α (TNF-α) and interleukin-18 (IL-18) production in LPS-stimulated PBMCs is due to the inhibition of the nuclear factor-κB activation pathway and/or inhibition of the processing pathway of pro-TNF-α and pro-IL-18, not to down-regulation of TLR-2 or TLR-4.
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Dizdarević-Hudić, Larisa, Zumreta Kušljugić, Fahir Baraković, Selmira Brkić, Damir Sabitović, Elmir Jahić, Maida Isabegović, Elnur Smajić, Igor Hudić, and Katarina Divković. "Correlation Between Interleukin 6 and Interleukin 10 in Acute Myocardial Infarction." Bosnian Journal of Basic Medical Sciences 9, no. 4 (November 20, 2009): 301–6. http://dx.doi.org/10.17305/bjbms.2009.2784.
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The aim of this study was to analyze (i) ratios between pro-inflammatory cytokines interleukin 6 (IL-6), interleukin 1 (IL-1), tumour necrosis factor α (TNF-α) and anti-inflammatory cytokine interleukin 10 (IL-10) in patients with acute myocardial infarction (AMI) and stable angina pectoris (ii) as well as correlation between IL-6 and IL-10 in AMI and (iii) correlation between IL-6 and lipoproteins in AMI.The total of 71 patients were enrolled in this study, 41 of them with AMI (study group) and 30 with stable angina pectoris (control group). The concentrations of cytokines and lipoproteins were measured from blood samples. Pro-inflammatory to anti-inflammatory cytokine ratios were calculated by dividing concentrations of pro-inflammatory cytokines with IL-10. In statistical analyses we used descriptive statistics, normality tests and analysis of correlation.IL-6: IL-10 ratio is significantly higher in AMI than in stable angina (P < 0,001), TNF-α: IL-10 is also higher in study group but the difference is not significant. We found positive linear correlation between IL-6 and IL-10 (r =0,43; p = 0,015) and negative linear correlation between IL-6 and high density lipoprotein HDL (r = -0,47; p= 0,008) in AMI.IL-6: IL-10 ratio is higher in AMI than in stable angina. There is linear correlation between IL-6 and IL-10 and IL-6 and HDL in AMI.
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Donato, Kevin A., Mélanie G. Gareau, Yu Jing Jenny Wang, and Philip M. Sherman. "Lactobacillus rhamnosus GG attenuates interferon-γ and tumour necrosis factor-α-induced barrier dysfunction and pro-inflammatory signalling." Microbiology 156, no. 11 (November 1, 2010): 3288–97. http://dx.doi.org/10.1099/mic.0.040139-0.
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The intestinal epithelium forms a protective barrier against luminal contents and the external environment, mediated via intercellular tight junctions (TJs). The TJ can be disrupted via cell signalling induced by either enteric pathogens or pro-inflammatory cytokines, thereby contributing to various intestinal disorders ranging from acute infectious diarrhoea to chronic inflammatory bowel diseases. Probiotics, such as Lactobacillus rhamnosus GG (LGG), are reported to confer beneficial effects on epithelial cells, including antagonizing infections and reducing overt pro-inflammatory responses, but the underlying mechanisms of these observed effects require further characterization. We hypothesized that probiotics preserve barrier function by interfering with pro-inflammatory cytokine signalling. Caco-2bbe cells were seeded into Transwells to attain polarized monolayers with intercellular TJs. Monolayers were inoculated apically with the probiotic LGG 3 h prior to the addition of IFN-γ (100 ng ml−1) to the basolateral medium overnight. The monolayers were then placed in fresh basal medium±TNF-α (10 ng ml−1) and transepithelial electrical resistance (TER) measurements were taken over the time-course of TNF-α stimulation. To complement the TER findings, cells were processed for zona occludens-1 (ZO-1) immunofluorescence staining. As a measure of TNF-α downstream signalling, cells were immunofluorescently stained for NF-κB p65 subunit and CXCL-8 mRNA was quantified by qRT-PCR. Basal cell culture medium was collected after overnight TNF-α stimulation to measure secreted chemokines, including CXCL-8 (interleukin-8) and CCL-11 (eotaxin). Following LGG inoculation, IFN-γ priming and 24 h TNF-α stimulation, epithelial cells maintained TER and ZO-1 distribution. LGG diminished the nuclear translocation of p65, demonstrated by both immunofluorescence and CXCL-8 mRNA expression. CXCL-8 and CCL-11 protein levels were decreased in LGG-inoculated, cytokine-challenged cells. These findings indicate that LGG alleviates the effects of pro-inflammatory cytokines on epithelial barrier integrity and inflammation, mediated, at least in part, through inhibition of NF-κB signalling.
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Zager, Richard A., Ali C. M. Johnson, and Steve Lund. "Uremia impacts renal inflammatory cytokine gene expression in the setting of experimental acute kidney injury." American Journal of Physiology-Renal Physiology 297, no. 4 (October 2009): F961—F970. http://dx.doi.org/10.1152/ajprenal.00381.2009.
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Inflammatory cytokines are evoked by acute kidney injury (AKI) and may contribute to evolving renal disease. However, the impact of AKI-induced uremia on proinflammatory (e.g., TNF-α, MCP-1, TGF-β1) and anti-inflammatory (e.g., IL-10) cytokine gene expression remains unknown. This study was undertaken to gain some initial insights into this issue. CD-1 mice were subjected to left renal ischemia-reperfusion (I/R) in the absence or presence of uremia (± right ureteral transection). TNF-α, MCP-1, TGF-β1, and IL-10 mRNAs, cytokine protein levels, and RNA polymerase II (Pol II) recruitment to these genes were assessed. Renal cytokine mRNA levels were also contrasted with unilateral vs. bilateral renal parenchymal damage (I/R or ureteral obstruction). Potential effects of uremia on cytokine mRNAs in the absence of parenchymal renal damage [bilateral ureteral transection (BUTx)] were sought. Finally, the impact of simulated in vitro uremia (HK-2 tubular cells exposed to peritoneal dialysate from uremic vs. normal mice) on cytokine mRNA and microRNA profiles was assessed. Uremia blunted TNF-α, MCP-1, and TGF-β1 mRNA increases in all three in vivo parenchymal acute renal failure models. These results were paralleled by reductions in cytokine protein levels and Pol II recruitment to their respective genes. Conversely, uremia increased IL-10 mRNA, both in the presence and absence (BUTx) of parenchymal renal damage. The uremic milieu also suppressed HK-2 cell proinflammatory cytokine mRNA levels and altered the expression of least 69 microRNAs ( P < 0.0001). We conclude that both pro- and anti-inflammatory cytokine gene expressions are influenced by uremia, with a potential predilection toward an anti-inflammatory state. Changes in gene transcription (as reflected by Pol II recruitment), and possible posttranscriptional modifications (known to be induced by microRNAs), are likely involved.
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Anuradha, Rajamanickam, Saravanan Munisankar, Yukti Bhootra, Jeeva Jagannathan, Chandrakumar Dolla, Paul Kumaran, Kui Shen, Thomas B. Nutman, and Subash Babu. "Systemic Cytokine Profiles in Strongyloides stercoralis Infection and Alterations following Treatment." Infection and Immunity 84, no. 2 (November 23, 2015): 425–31. http://dx.doi.org/10.1128/iai.01354-15.
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Strongyloides stercoralisis a soil-transmitted helminth organism that infects ∼50 to 100 million people worldwide. Despite its widespread prevalence, very little is known about the immune response that characterizes humanS. stercoralisinfection. To study the systemic cytokine profile characteristic ofStrongyloidesinfection, we measured the circulating levels of a large panel of pro- and anti-inflammatory cytokines in asymptomatic, infected individuals (n= 32) and compared them to those in uninfected, controls (n= 24). Infected individuals exhibited significantly lower circulating levels of proinflammatory cytokines (gamma interferon [IFN-γ], tumor necrosis factor alpha [TNF-α], and interleukin-1β [IL-1β]) and significantly higher levels of anti-inflammatory cytokines (IL-4, IL-5, IL-9, IL-10, IL-13, IL-27, IL-37, and transforming growth factor β [TGF-β]). Moreover, treatment ofStrongyloidesinfection resulted in a significant reversal of the cytokine profile, with increased levels of proinflammatory (IFN-γ, TNF-α, IL-2, IL-17A, IL-17F, IL-22, IL-23, and IL-1β) and decreased levels of anti-inflammatory (IL-4, IL-5, IL-9, IL-10, IL-13, IL-27, IL-37, and TGF-β) cytokines following treatment. Thus,S. stercoralisinfection is characterized by alterations in the levels of systemic cytokines, reflecting major alterations in the underlying immune response to this chronic helminth infection.
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Molnár, T., B. Jójárt, T. Resál, K. Szántó, D. Kata, I. Földesi, T. Molnár, J. Maléth, and K. Farkas. "P065 Determination of the cytokine pattern of human colon organoids derived from Inflammatory Bowel Disease patients." Journal of Crohn's and Colitis 16, Supplement_1 (January 1, 2022): i173. http://dx.doi.org/10.1093/ecco-jcc/jjab232.194.
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Abstract Background Inflammatory bowel diseases (IBD) are characterized by chronic inflammation of the gastrointestinal tract which is associated with imbalanced pro- and anti-inflammatory cytokines. Anti-TNF-α therapy is widely used, but 10–30% of the patients are primarily not responding to the treatment or lose response over time. In vitro organoid cultures (OCs) generated from tissue specific adult stem cells can mimic cellular diversity and function of the organ of origin and might be used as a predictive tool for patient specific therapeutic response. However, the reductionist nature of the OCs and lack of knowledge about the proper representation of the disease features currently limit the utilization of the OCs as ex vivo IBD models. Methods Therefore our aims were to determine and compare cytokine profiles of colonic biopsies collected from IBD patients and OCs generated from the same biopsies, and to follow the changes of cytokine expression over time. In this study samples from 20 IBD and 8 non-IBD patients were used. Biopsies were taken during colonoscopy from inflamed part of the colon of IBD patients. Crypts were isolated from biopsy samples to establish colon OCs. Total protein and RNA were isolated from biopsies and OCs. Cytokine Array was used to determine cytokine patterns in our samples. Gene expressions of control and IBD OCs after first passage was compared by qPCR. TNF-α concentrations and cellular expression was determined by EILSA and immunostainings, respectively in control and IBD OCs. To determine therapeutic response OCs were treated with anti-TNF-α therapy. Results Cytokine patterns of colon biopsies and OCs were remarkably similar until first passage. The major pro-inflammatory cytokines, IL-1β, IL-6, IL-8, were detected both in biopsies and OCs. After second passage the cytokine expression decreased or disappeared in OCs. TNF-α was also measurable in the OCs, however a similar decrease was observed, which was also confirmed by immunostaining. Gene expression analysis in IBD OCs showed an increased TNF-α, IL-1β and IL-6 levels compared to healthy control OCs after first passage. ELISA also showed higher TNF-α concentration in organoids from inflamed origin compared to controls. After anti-TNF-α treatment we detected a decrease in the IL-6 gene expression in treated OCs. Conclusion Our results suggest that colon OCs maintain the cytokine expression ex vivo until the 2nd passage and show inflammatory characteristics. Moreover, in vitro treatment induces changes in the cytokine expression. Based on these results the utility of patient-derived organoids to predict the therapeutic response can be investigated.
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Salmeri, Francesca Maria, Lucia Denaro, Elisa Ruello, Giuseppe Acri, Sergio Gurgone, Carlo Sansotta, and Barbara Testagrossa. "Irradiation with Polychromatic Incoherent Low Energy Radiation of Human Peripheral Blood Mononuclear Cells In Vitro: Effects on Cytokine Production." International Journal of Environmental Research and Public Health 17, no. 4 (February 14, 2020): 1233. http://dx.doi.org/10.3390/ijerph17041233.
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(1) Background: Physical stimuli may activate peripheral blood mononuclear cells (PBMCs) to secrete cytokines, which may favor pro-inflammatory responses or trigger reparative phenomena. The purpose of this study is to evaluate the action of Polarized Polychromatic Incoherent Low Energy Radiation (PILER) on human in vitro PBMCs, by detection of the possible effects on cytokine production; (2) Methods: isolated PBMCs were irradiated with a PILER lamp at different exposure times, at a distance of 10 cm, before incubation. The supernatants were collected after 24 h and 48 h and cytokines evaluated by ELISA; (3) Results: Our results showed a decrease in the levels of pro-inflammatory IL-12p70, IL-17A, IFN-γ, and TNF-α cytokines, whereas IL-10 and TGF-β1 with regulatory activity increased; (4) Conclusions: PILER irradiation affected the cytokine production by isolated PBMCs driving the immune response toward an anti-inflammatory/reparative profile.
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Simons, Peter J., Petra S. van den Pangaart, Johannes M. F. G. Aerts, and Louis Boon. "Pro-inflammatory delipidizing cytokines reduce adiponectin secretion from human adipocytes without affecting adiponectin oligomerization." Journal of Endocrinology 192, no. 2 (February 2007): 289–99. http://dx.doi.org/10.1677/joe-06-0047.
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Adiponectin and, especially, its oligomeric complex composition have been suggested to be critical in determining insulin sensitivity. Pro-inflammatory cytokines play an important role in the development of insulin resistance in obesity and associated diseases. Therefore, we investigated the effect of long-term exposure of tumour necrosis factor (TNF)-α, interleukin (IL)-6, IL-1β, and interferon (IFN)-γ on total insulin-sensitizing adiponectin secretion and adiponectin complex formation from human adipocytes. In parallel, adipocyte delipidation and leptin production levels were monitored. The present study demonstrates that TNF-α, IL-1β, and IFN-γ dose and time dependently suppressed total adiponectin secretion within 7 days (60, 70, and 35% reduction respectively). IL-6 was also able to reduce (50%) adiponectin production, although only in combination with exogenous soluble IL-6 receptors (sIL-6R). However, the oligomeric distribution (high, middle, and low molecular weight (HMW) complexes) of secreted adiponectin was not altered by any of these cytokines. All studied pro-inflammatory cytokines resulted in delipidation and reduction of lipid-laden adipocyte numbers. Despite this reduction of lipid-laden adipocytes, TNF-α, IL-6/sIL-6R, and IL-1β stimulated leptin release. Our data indicate that (i) long-term pro-inflammatory cytokine exposure downregulates total adiponectin secretion from delipidizing adipocytes and (ii) pro-inflammatory cytokines are not important regulators of adipocyte-derived adiponectin oligomerization. Hence, their individual contribution to low expression of HMW adiponectin found in insulin-resistant conditions seems unlikely. Furthermore, delipidizing adipocytes and preadipocytes are active leptin producers when stimulated by TNF-α, IL-6/sIL-6R, and IL-1β.
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Xu, Li-Ying, Wan-Ru Cai, Chun-Fang Ma, Qi-Yang Shou, Jing-Li Qian, and Turan S. Huseyin. "Qi-Dong-Huo-Xue-Yin Inhibits Inflammation in Acute Lung Injury in Mice via Toll-Like Receptor 4/Caveolin-1 Signaling." Evidence-Based Complementary and Alternative Medicine 2018 (2018): 1–11. http://dx.doi.org/10.1155/2018/2373609.
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Acute lung injury (ALI) is a critical illness with no current effective treatment. Caveolin-1 indirectly activates inflammation-associated signaling pathways by inhibiting endothelial nitric oxide synthase (eNOS). This induces an imbalance between pro- and anti-inflammatory cytokine levels, which are involved in the pathogenesis of ALI. The compound Chinese prescription Qi-Dong-Huo-Xue-Yin (QDHXY) is efficacious for ALI treatment via an anti-inflammatory effect; however, the exact underlying mechanism is unknown. Therefore, we explored the protective effect of QDHXY against lipopolysaccharide- (LPS-) induced ALI in mice. Histopathological changes in mouse lung tissues were studied. Furthermore, alterations in the serum levels of pro- and anti-inflammatory cytokines were investigated. The levels of tumor necrosis factor- (TNF-)α, interleukin- (IL-) 6, IL-1β, and interferon-γ-induced protein 10 in bronchoalveolar lavage fluid were measured. Additionally, the expression levels of myeloid differentiation factor 88 (MyD88), caveolin-1, and eNOS were assessed. QDHXY significantly reduced lung infiltration with inflammatory cells and the production of serum pro- and anti-inflammatory cytokines and inhibited the expression of TNF-α, IL-1β, caveolin-1, and MyD88 but not eNOS. These indicate that QDHXY significantly improved the balance between pro- and anti-inflammatory cytokine levels, possibly by inhibiting the caveolin-1 signaling pathway. Therefore, QDHXY may be a potential treatment for ALI.
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Chen, Xia, Min Xiu, Juanjuan Xing, Shaoqing Yu, Dinghong Min, and Fei Guo. "Lanthanum Chloride Inhibits LPS Mediated Expressions of Pro-Inflammatory Cytokines and Adhesion Molecules in HUVECs: Involvement of NF-κB-Jmjd3 Signaling." Cellular Physiology and Biochemistry 42, no. 5 (2017): 1713–24. http://dx.doi.org/10.1159/000479439.
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Background/Aims: To investigate the regulation of LaCl3 on lipopolysaccharides (LPS)-induced pro-inflammatory cytokines and adhesion molecules in human umbilical vein endothelial cells (HUVECs). Methods: Primary cultured HUVECs were pretreated with 2.5 µM LaCl3 for 30 min followed by 1 µg/ml LPS for 2 h. Pro-inflammatory cytokine and adhesion molecule expressions were determined by real-time RT-PCR and ELISA. NF-κB/p65 nuclear translocation was examined by immunofluorescence and immuno-blot, and its DNA-binding activity was measured by chemiluminescence. Recruitment of NF-κB/p65, Jmjd3, and H3K27me3 to gene promoter regions was determined by ChIP-qPCR. Results: LaCl3 exhibited no cytotoxic effects to primary HUVECs at concentrations ≤ 50 µM. LPS-mediated TNF-α, IL-1β, IL-6, MMP-9, and ICAM-1 production, nuclear translocation, and DNA-binding activity of NF-κB/p65, as well as Jmjd3 expression, were all reduced significantly by LaCl3. Furthermore, LaCl3 treatment significantly impaired LPS-induced enrichment of NF-κB/p65 to the promoter regions of TNF-α, MMP-9, IL-1β, ICAM-1, and IL-6; and of Jmjd3 to the promoter regions of TNF-α, MMP-9, IL-1β, and IL-6. H3K27me3 abundance in the promoter regions of TNF-α and ICAM-1 increased significantly in following LaCl3 treatment. Conclusion: LaCl3 inhibits pro-inflammatory cytokine and adhesion molecule expressions induced by LPS in HUVECs. NF-κB and histone demethylase Jmjd3 are involved in this effect.
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Molnár, T., B. Jójárt, T. Resál, K. Szántó, D. Kata, I. Földesi, T. Molnár, J. Maléth, and K. Farkas. "P046 Disease modelling of Inflammatory Bowel Disease by human colon organoids." Journal of Crohn's and Colitis 15, Supplement_1 (May 1, 2021): S155. http://dx.doi.org/10.1093/ecco-jcc/jjab076.175.
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Abstract Background Inflammatory bowel diseases (IBD) are characterized by chronic inflammation of the gastrointestinal tract which is associated with the imbalanced pro- and anti-inflammatory cytokines. Anti-TNF-α is widely used as a therapeutic agent, but 10–30% of the patients are not responding to the treatment or in time it become less affective. In vitro organoid cultures generated from stem cells can mimic the cellular diversity and function of the organ of origin and might be used as a predictive tool for patient specific response. However, the in vitro cytokine expression pattern of the IBD colon organoid cultures have never been determined or compared with the cytokine expression of the colon mucosa. Methods Our aim was to determine and compare the cytokine profiles of the colon biopsy samples in IBD patients and organoid cultures generated from these biopsies. In this study samples from 5 IBD patients were used. Biopsies were taken during colonoscopy from inflamed part of the colon. Crypts were isolated from the biopsy samples to start colon organoid culture. Total protein was isolated from the biopsies and the organoids. Cytokine Array was used to determine the cytokine patterns in both samples. ELISA was used to measure the TNF-α concentrations and immunofluorescence staining to localize it in the organoids. Results We determined the cytokine profile of the biopsy samples and the colon organoid cultures. The cytokine patterns were remarkably similar until the first passage. The major pro-inflammatory cytokines, IL-1β, IL-6, IL-8, were detected in the organoids after the first passage. After the second passage the cytokine expression decreased or disappeared. ELISA revealed that TNF-α was also expressed in the organoid cultures, however a similar decrease in the expression was observed, which was also confirmed by immunofluorescence staining. TNF-α positive cells were present in the organoids, but it decreased after every passage. Conclusion Our results suggest that the colon organoid cultures maintain the cytokine profile of the tissue of origin until a limited time (until the first passage). Therefore, organoids might be used to determine patient specific therapy for drug tests.
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Beklen, A., M. Laine, I. Ventä, T. Hyrkäs, and Y. T. Konttinen. "Role of TNF-α and Its Receptors in Pericoronitis." Journal of Dental Research 84, no. 12 (December 2005): 1178–82. http://dx.doi.org/10.1177/154405910508401216.
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The classic stimulus for cellular cytokine production is bacterial lipopolysaccharide (endotoxin). It was therefore hypothesized that tumor necrosis factor-α (TNF-α) may be responsible for pericoronitis. TNF-α and its receptors were detected by immunohistochemical staining in third molar pericoronitis in ten patients and ten healthy control samples. The percentage of TNF-α positive cells was high in pericoronitis (p = 0.0317). TNF receptors TNF-R1 and TNF-R2 were found in macrophage- and fibroblast-like cells, vascular endothelial cells in post-capillary venules, and basal epithelial cells in pericoronitis, but were only weakly expressed in controls. Increased expression of interleukin-1β and vascular cell adhesion molecule-1 was found as a biological indicator of TNF-α ligand-receptor interaction. Explanted tissues acquired destructive potential upon TNF-α stimulation, whereas TNF-α blockers controlled it in inflamed tissues. These findings suggest that, in pericoronitis, inflammatory and resident cells produce and respond to potent pro-inflammatory cytokine TNF-α, with pathogenic and potential therapeutic relevance.
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Behm, Christian, Alice Blufstein, Johannes Gahn, Barbara Kubin, Michael Nemec, Andreas Moritz, Xiaohui Rausch-Fan, and Oleh Andrukhov. "1,25(OH)2D3 Differently Affects Immunomodulatory Activities of Mesenchymal Stem Cells Depending on the Presence of TNF-α, IL-1β and IFN-γ." Journal of Clinical Medicine 8, no. 12 (December 14, 2019): 2211. http://dx.doi.org/10.3390/jcm8122211.
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Periodontal ligament-derived mesenchymal stem cells (hPDLSCs) possess immunomodulatory abilities which are strongly enhanced by various inflammatory cytokines. Vitamin D3 has anti-inflammatory effects on hPDLSCs and immune cells. However, no study to date has directly compared the influence of 1,25(OH)2D3 on the immunomodulatory activities of hPDLSCs in the presence of different cytokines. In the present study, the effects of hPDLSCs treated with tumor necrosis factor (TNF)-α, interleukin (IL)-1β, or interferon (IFN)-γ in the presence of 1,25(OH)2D3 on the proliferation of allogenic CD4+ T lymphocyte or on the functional status of primary CD68+ macrophages were analyzed in coculture models. Additionally, the effects of 1,25(OH)2D3 on TNF-α-, IL-1β-, and IFN-γ-induced gene expression of some immunomodulatory factors in hPDLSCs were compared. Under coculture conditions, 1,25(OH)2D3 increased or decreased CD4+ T lymphocyte proliferation via hPDLSCs, depending on the cytokine. hPDLSCs primed with 1,25(OH)2D3 and different cytokines affected pro- and anti-inflammatory cytokine expression in macrophages variably, depending on the priming cytokine. With one exception, 1,25(OH)2D3 significantly reduced TNF-α-, IL-1β-, and IFN-γ-induced expression of all the investigated immunomediators in hPDLSCs, albeit to different extents. These results suggest that 1,25(OH)2D3 influences the immunomodulatory activities of hPDLSCs depending qualitatively and quantitatively on the presence of certain inflammatory cytokines.
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Vidya G Doddawad, Vidya CS, Shivananda S, B.M. Gurupadayya, Divya Rao, and H.Hari Kishore Bhat. "Expression of TNF-α in oral cancer: A prospective diagnostic and prognostic molecular biomarker." Journal of Pharmaceutical Negative Results 13, no. 4 (November 24, 2022): 1384–90. http://dx.doi.org/10.47750/pnr.2022.13.04.193.
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TNF-α is a multifunctional cytokine that regulates cell proliferation and differentiation, as well as immunological and host defense responses to infection. It also induces angiogenesis, modulates tissue remodeling, and controls apoptosis.TNF-α is a pleiotropic, pro-inflammatory cytokine that has the potential to be both pro-tumorigenic and anti-tumorigenic. TNF-α can be cytotoxic to tumour cells, slowing tumour progression or causing necrosis, and it can also enhance angiogenesis, proliferation, migration, and survival of tumour cells in oral cancer cells. Several research studies clearly imply that TNF-α and its soluble receptors could be effective in detecting, staging, and predicting prognosis in a variety of malignancies, including oral tumours. Well in many studies were conducted to detect the actual response of TNF- α, but lack of knowledge in understanding the true response of TNF-α towards oral precancer and oral cancer
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Hickman-Brown, Kyle J., Molly S. Smith, Brooke E. McAnally, Ramiro V. Oliveira Filho, Gabriela Dalmaso de Melo, Ky G. Pohler, and Rebecca K. Poole. "PSV-B-16 Correlation between Plasma, Uterine, and Vaginal Cytokine Concentrations in Postpartum Beef Cows Prior to Artificial Insemination." Journal of Animal Science 100, Supplement_3 (September 21, 2022): 347–48. http://dx.doi.org/10.1093/jas/skac247.635.
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Abstract Cytokines have a vital role in reproductive immune environment during the postpartum period. Previous data evaluated uterine and vaginal cytokine concentrations prior to insemination; however, was unable to correlate these data with plasma cytokine concentrations. The objective of this study was to determine relationships between uterine, vaginal, and plasma pro- and anti-inflammatory cytokine concentrations in postpartum beef cows prior to timed artificial insemination (TAI). Bos indicus-influenced beef cows (n=20) free of any physical, health or reproductive-related issues were subjected to the Bee Synch II protocol 8 days prior (d-8) to TAI (d0). Uterine and vaginal flushes and blood were collected on d-3 and d-1. Pregnancy was determined by transrectal ultrasonography on d28 (Pregnant, n=7; Open, n=13). Using the RayBiotech Quantibody Bovine Cytokine Array 1 the following cytokines concentrations were determined: interferon (IFN)-α, IFN-γ, interleukin (IL)-13, IL-1α, IL-1-F5, IL-21, tumor necrosis factor (TNF)-α, chemokine ligand (CXCL)-9, CXCL-10, and chemokine ligand 4 (CCL4). Concentration data were analyzed using PROC GLM and correlations using Pearson correlation in SAS. For plasma samples, 8 pro-inflammatory cytokines (IFN-α, IFN-γ, IL-13, IL-1α, IL-1-F5, IL-21, CXCL-9, and TNF-α) had greater (P< 0.05) concentrations in open cows compared with pregnant cows. For uterine flushes, 3 pro-inflammatory cytokines (IFN-γ, IL-1α, and IL-21) had greater (P< 0.05) concentrations in open cows compared with pregnant cows. For vaginal flushes, IFN-α concentrations were greater (P< 0.05) in open cows, while CXCL-10 concentrations were greater in pregnant cows. There were no significant correlations between plasma and uterine or vaginal samples (P>0.05). Interestingly, for open cows there were correlations for IFN-α (r=0.46; P=0.02), IFN-γ (r=0.58; P=0.002), and IL-21 (r=0.54; P=0.004) between uterine and vaginal samples; however, no correlations were observed for pregnant cows. These results suggest a greater abundance of pro-inflammatory cytokines within the uterus, vagina, and in peripheral circulation for resulting open cows prior to TAI.
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Kwiatek, Maciej, Tomasz Gęca, and Anna Kwaśniewska. "Pro- and Anti-Inflammatory Cytokines in the First Trimester—Comparison of Missed Miscarriage and Normal Pregnancy." International Journal of Environmental Research and Public Health 18, no. 16 (August 12, 2021): 8538. http://dx.doi.org/10.3390/ijerph18168538.
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The advantage in response of Th2 over Th1 is observed in normal pregnancy in peripheral blood. A disturbance of this balance can lead to symptoms of miscarriage and pregnancy loss. The aim of this study was to evaluate the pro- and anti-inflammatory cytokines in sera of women who were diagnosed with missed miscarriage in the first trimester and to compare this systemic immune response to the response in women with normal pregnancy. The study group consisted of 61 patients diagnosed with missed miscarriage. In total, 19 healthy women with uncomplicated first trimester created the control group. Cytokines were determined in the maternal serum by ELISA. The analysis included INF-γ, TNF-α, Il-1β, Il-4, Il-5, Il-6, Il-9, Il-10, Il-13 and TGF-β1. Th1 cytokine levels in the study group reached slightly higher values for INF-γ, Il-1β and slightly lower for IL-6 and TNF-α. In turn, Th2 cytokine levels in the study group were slightly higher (Il-9, Il-13), significantly higher (Il4, p = 0.015; Il-5, p = 0.0003) or showed no differences with the control group (Il-10). Slightly lower concentration involved only TGF-β1. Analysis of the correlation between levels of pro- and anti-inflammatory cytokines resulted in some discrepancies, without showing predominance of a specific immune response. The results did not confirm that women with missed miscarriage had an advantage in any type of immune response in comparison to women with normal pregnancy.
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Samancı, Bedia, Yavuz Samancı, Erdem Tüzün, Güneş Altıokka-Uzun, Esme Ekizoğlu, Sema İçöz, Erdi Şahin, Cem İsmail Küçükali, and Betül Baykan. "Evidence for potential involvement of pro-inflammatory adipokines in the pathogenesis of idiopathic intracranial hypertension." Cephalalgia 37, no. 6 (May 18, 2016): 525–31. http://dx.doi.org/10.1177/0333102416650705.
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Background Although specific role players are currently unknown, contribution of inflammatory mediators has been suggested in the pathophysiology of idiopathic intracranial hypertension (IIH), which is a disease more prevalent in obese female individuals of childbearing age. We aimed to investigate the levels of adipokines and cytokines to demonstrate possible markers for inflammation that participate in IIH pathophysiology and their association with clinical features of IIH. Methods IIH patients, diagnosed according to the revised criteria, and age-, gender- and body mass index (BMI)-matched healthy controls were enrolled in this study. Serum samples were evaluated for insulin-like growth factor 1, insulin, nesfatin, adiponectin, interleukin (IL)-1β, IL-6, IL-8, leptin, plasminogen activator inhibitor type-1, resistin, tumour necrosis factor-alpha (TNF-α) and monocyte chemotactic protein 1 via enzyme-linked immunosorbent assay or multiplex immunoassays. Results IL-1β level was significantly higher ( p = 0.012), and IL-8 and TNF-α levels were significantly lower in the IIH group ( p < 0.001 and p = 0.008, respectively) compared to the control group. There were no correlations between the cytokine/adipokine levels and age, BMI, disease duration, and cerebrospinal fluid oligoclonal bands. There were also no significant differences in cytokine and adipokine levels between IIH patients regarding visual impairment. However, statistically significant differences were found between IIH patients with relapse versus healthy controls regarding IL-1β ( p = 0.007), IL-8 ( p = 0.001) and TNF-α ( p = 0.017) levels. Other investigated cytokines and adipokines showed no significant alterations in IIH patients investigated in the remission period. Conclusion Altered serum levels of IL-1β, IL-8 and TNF-α seem to be associated with IIH pathogenesis, and these cytokines may be used as prognostic markers in IIH to predict relapse.
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Gaglio, Salvatore Calogero, Marta Donini, Piyachat Evelyn Denbaes, Stefano Dusi, and Massimiliano Perduca. "Oxyresveratrol Inhibits R848-Induced Pro-Inflammatory Mediators Release by Human Dendritic Cells Even When Embedded in PLGA Nanoparticles." Molecules 26, no. 8 (April 7, 2021): 2106. http://dx.doi.org/10.3390/molecules26082106.
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Oxyresveratrol, a stilbene extracted from the plant Artocarpus lakoocha Roxb., has been reported to provide a considerable anti-inflammatory activity. Since the mechanisms of this therapeutic action have been poorly clarified, we investigated whether oxyresveratrol affects the release of the pro-inflammatory cytokines IL-12, IL-6, and TNF-α by human dendritic cells (DCs). We found that oxyresveratrol did not elicit per se the release of these cytokines, but inhibited their secretion induced upon DC stimulation with R848 (Resiquimod), a well-known immune cell activator engaging receptors recognizing RNA viruses. We then investigated whether the inclusion of oxyresveratrol into nanoparticles promoting its ingestion by DCs could favor its effects on cytokine release. For this purpose we synthesized and characterized poly(lactic-co-glycolic acid) (PLGA) nanoparticles, and we assessed their effects on DCs. We found that bare PLGA nanoparticles did not affect cytokine secretion by resting DCs, but increased IL-12, IL-6, and TNF-α secretion by R848-stimulated DCs, an event known as “priming effect”. We then loaded PLGA nanoparticles with oxyresveratrol and we observed that oxyresveratrol-bearing particles did not stimulate the cytokine release by resting DCs and inhibited the PLGA-dependent enhancement of IL-12, IL-6, and TNF-α secretion by R848-stimulated DCs. The results herein reported indicate that oxyresveratrol suppresses the cytokine production by activated DCs, thus representing a good anti-inflammatory and immune-suppressive agent. Moreover, its inclusion into PLGA nanoparticles mitigates the pro-inflammatory effects due to cooperation between nanoparticles and R848 in cytokine release. Therefore, oxyresveratrol can be able to contrast the synergistic effects of nanoparticles with microorganisms that could be present in the patient tissues, therefore overcoming a condition unfavorable to the use of some nanoparticles in biological systems.
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Mahaki, Hanie, Naghi Jabarivasal, Khosro Sardarian, and Alireza Zamani. "Effects of Various Densities of 50 Hz Electromagnetic Field on Serum IL-9, IL-10, and TNF-α Levels." International Journal of Occupational and Environmental Medicine 11, no. 1 (October 1, 2020): 24–32. http://dx.doi.org/10.15171/ijoem.2020.1572.
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Background: Extremely low-frequency electromagnetic fields (ELF-EMFs) are abundantly produced in modern societies. In recent years, interest in the possible effects of ELF-EMFs on the immune system has progressively increased. Objective: To examine the effects of ELF-EMFs with magnetic flux densities of 1, 100, 500, and 2000 µT on the serum levels of interleukin (IL)-9, IL-10, and tumor necrosis factor-alpha (TNF-α). Methods: 80 adult male rats were exposed to ELF-EMFs at a frequency of 50 Hz for 2 h/day for 60 days. The serum cytokines were measured at two phases of pre- and post-stimulation of the immune system by human serum albumin (HSA). Results: Serum levels of IL-9 and TNF-α, as pro-inflammatory cytokines, were decreased due to 50 Hz EMFs exposure compared with the controls in the pre- and post-stimulation phases. On the contrary, exposures to 1 and 100 µT 50 Hz EMFs increased the levels of antiinflammatory cytokine, and IL-10 only in the pre-stimulation phase. In the post-stimulation phase, the mean level of serum IL-10 was not changed in the experimental groups. Conclusion: The magnetic flux densities of 1 and 100 µT 50 Hz EMFs had more immunological effects than EMFs with higher densities. Exposure to 50 Hz EMFs may activate anti-inflammatory effects in rats, by down-modulation of pro-inflammatory cytokines (IL-9 and TNF-α) and induction of the anti-inflammatory cytokine (IL-10).
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Novikov, A. A., Е. N. Aleksandrova, and G. V. Lukina. "Serum cytokine profile in early and established rheumatoid arthritis." Almanac of Clinical Medicine 47, no. 5 (November 13, 2019): 393–99. http://dx.doi.org/10.18786/2072-0505-2019-47-058.
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Background: An important characteristic of immune pathology in rheumatoid arthritis (RA) is a B-cell tolerance defect, associated with autoantibodies production, and antigen-specific activation of Th-1 CD4+ T lymphocytes with an excess production of pro-inflammatory cytokines compared to anti-inflammatory ones. Pro-inflammatory cytokines contribute to the development of local inflammatory effects, induce bone destruction and pannus formation, and contribute to the development of autoimmune abnormalities and systemic manifestations. Anti-inflammatory cytokines are able to reduce the rate of joint destruction. There is evidence of the involvement of Th2 cytokines in the development of early RA. These facts suggest the need for a thorough investigation into the balance between the Th1 and Th2 types of immune response at different stages of the disease.Aim: To assess the importance of сytokine profiling in the evaluation of immune abnormalities in RA.Materials and methods: In this descriptive, controlled, retrospective study, we examined 118 patients with RA and 33 healthy donors as a control group. Serum IgM rheumatoid factor (RF) and C-reactive protein (CRP) levels were measured by immunonephelometry; anti-cyclic citrullinated peptide antibodies (anti-CCP) and anti-mutated citrullinated vimentin antibodies (anti-MCV) were determined by an enzyme immunoassay, cytokines levels with "xMAP" technique.Results: Serum cytokine levels vary depending on RA duration. The cytokine profile in early RA, unlike that in established RA with a duration of more than 6 months, is characterized by higher levels of pro-inflammatory (MIP-1α), Th1 (IFN-γ), and Th17 (IL-17) cytokines, colony-stimulating factors (IL-7, G-CSF), and chemokines (IL-8, IP-10) (p < 0.05 for all parameters). In established RA, the levels of pro-inflammatory (IL-1β, -6, -15, TNF-α), anti-inflammatory (IL-1ra, IL-10, IL-13, IL-5), Th1 (IL-2, IL-12), Th2 (IL-9) cytokines and colony-stimulating factors (G-CSF, GM-CSF) correlate with the concentrations of IgM RF and antibodies to citrullinated proteins (antiCCP, anti-MCV) (all p < 0.05). There was also а correlation between CRP and pro-inflammatory (IL-1β, IL-6, TNF-α), Th1 (IL-12), Th2 (IL-5, IL-9) cytokine levels and between DAS28 and pro-inflammatory cytokine (IL-6) and colony-stimulating factor (G-CSF) levels (all p < 0.05). Conclusion: In RA, cytokines, chemokines and colony-stimulating factors mirror the inflammatory activity of the disease. Changes in blood concentrations of cytokines enable to get an insight into the complex interplay of numerous mediators of innate and acquired immunity
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Shah, Jay H., I. S. Anand, and K. K. Shah. "Inhibition of Pro-Inflammatory Cytokine TNF-α by Boerhaavia diffusa (L.) in Liposaccharide stimulated Human THP-1 cells." International Journal of Research and Development in Pharmacy and Life Sciences 6, no. 6 (November 2017): 2820–23. http://dx.doi.org/10.21276/ijrdpl.2278-0238.2017.6(6).2820-2823.
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Harazin, András, Alexandra Bocsik, Lilla Barna, András Kincses, Judit Váradi, Ferenc Fenyvesi, Vilmos Tubak, Maria A. Deli, and Miklós Vecsernyés. "Protection of cultured brain endothelial cells from cytokine-induced damage by α-melanocyte stimulating hormone." PeerJ 6 (May 15, 2018): e4774. http://dx.doi.org/10.7717/peerj.4774.
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The blood–brain barrier (BBB), an interface between the systemic circulation and the nervous system, can be a target of cytokines in inflammatory conditions. Pro-inflammatory cytokines tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) induce damage in brain endothelial cells and BBB dysfunction which contribute to neuronal injury. The neuroprotective effects of α-melanocyte stimulating hormone (α-MSH) were investigated in experimental models, but there are no data related to the BBB. Based on our recent study, in which α-MSH reduced barrier dysfunction in human intestinal epithelial cells induced by TNF-α and IL-1β, we hypothesized a protective effect of α-MSH on brain endothelial cells. We examined the effect of these two pro-inflammatory cytokines, and the neuropeptide α-MSH on a culture model of the BBB, primary rat brain endothelial cells co-cultured with rat brain pericytes and glial cells. We demonstrated the expression of melanocortin-1 receptor in isolated rat brain microvessels and cultured brain endothelial cells by RT-PCR and immunohistochemistry. TNF-α and IL-1β induced cell damage, measured by impedance and MTT assay, which was attenuated by α-MSH (1 and 10 pM). The peptide inhibited the cytokine-induced increase in brain endothelial permeability, and restored the morphological changes in cellular junctions visualized by immunostaining for claudin-5 and β-catenin. Elevated production of reactive oxygen species and the nuclear translocation of NF-κB were also reduced by α-MSH in brain endothelial cells stimulated by cytokines. We demonstrated for the first time the direct beneficial effect of α-MSH on cultured brain endothelial cells, indicating that this neurohormone may be protective at the BBB.
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Cereda, CW, C. Zecca, L. Mazzucchelli, L. Valci, C. Staedler, CL Bassetti, and C. Gobbi. "Tumefactive demyelinating lesions during etanercept treatment requiring decompressive hemicraniectomy." Multiple Sclerosis Journal 19, no. 6 (October 15, 2012): 820–23. http://dx.doi.org/10.1177/1352458512461969.
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Tumor necrosis factor alpha (TNF-α) is a pro-inflammatory and immunoregulatory cytokine involved in the pathogenesis of several autoimmune disorders. Etanercept, a TNF-α antagonist (anti-TNF-α) acting as a soluble TNF-α receptor, has been associated with neurological demyelinating disorders. This paper aims to report an unusual case showing tumefactive central nervous system (CNS) inflammatory demyelination in a patient in the course of TNF -α antagonist therapy, requiring decompressive hemicraniectomy. This report is based on magnetic resonance imaging (MRI) findings and histology. A biopsy confirmed the inflammatory demyelinating nature of the lesions. The clinical presentation is unusual due to the severity of the disease process, requiring decompressive hemicraniotomy with a clinically favorable outcome.
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Wang, Zhiyu, Yanfei Wang, Prachi Vilekar, Seung-Pil Yang, Mayuri Gupta, Myong In Oh, Autumn Meek, et al. "Small molecule therapeutics for COVID-19: repurposing of inhaled furosemide." PeerJ 8 (July 7, 2020): e9533. http://dx.doi.org/10.7717/peerj.9533.
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The novel coronavirus SARS-CoV-2 has become a global health concern. The morbidity and mortality of the potentially lethal infection caused by this virus arise from the initial viral infection and the subsequent host inflammatory response. The latter may lead to excessive release of pro-inflammatory cytokines, IL-6 and IL-8, as well as TNF-α ultimately culminating in hypercytokinemia (“cytokine storm”). To address this immuno-inflammatory pathogenesis, multiple clinical trials have been proposed to evaluate anti-inflammatory biologic therapies targeting specific cytokines. However, despite the obvious clinical utility of such biologics, their specific applicability to COVID-19 has multiple drawbacks, including they target only one of the multiple cytokines involved in COVID-19’s immunopathy. Therefore, we set out to identify a small molecule with broad-spectrum anti-inflammatory mechanism of action targeting multiple cytokines of innate immunity. In this study, a library of small molecules endogenous to the human body was assembled, subjected to in silico molecular docking simulations and a focused in vitro screen to identify anti-pro-inflammatory activity via interleukin inhibition. This has enabled us to identify the loop diuretic furosemide as a candidate molecule. To pre-clinically evaluate furosemide as a putative COVID-19 therapeutic, we studied its anti-inflammatory activity on RAW264.7, THP-1 and SIM-A9 cell lines stimulated by lipopolysaccharide (LPS). Upon treatment with furosemide, LPS-induced production of pro-inflammatory cytokines was reduced, indicating that furosemide suppresses the M1 polarization, including IL-6 and TNF-α release. In addition, we found that furosemide promotes the production of anti-inflammatory cytokine products (IL-1RA, arginase), indicating M2 polarization. Accordingly, we conclude that furosemide is a reasonably potent inhibitor of IL-6 and TNF-α that is also safe, inexpensive and well-studied. Our pre-clinical data suggest that it may be a candidate for repurposing as an inhaled therapy against COVID-19.
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FITZGERALD, PETER, SINEAD M. O'BRIEN, PAUL SCULLY, KIM RIJKERS, LUCINDA V. SCOTT, and TIMOTHY G. DINAN. "Cutaneous glucocorticoid receptor sensitivity and pro-inflammatory cytokine levels in antidepressant-resistant depression." Psychological Medicine 36, no. 1 (October 28, 2005): 37–43. http://dx.doi.org/10.1017/s003329170500632x.
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Background. There is evidence to indicate that peripheral glucocorticoid receptor (GR) function is reduced in major depression, and a possible molecular explanation for this is the impact of raised pro-inflammatory cytokines. The topical steroid vasoconstriction assay provides a convenient probe of peripheral GR function. The present study sought to assess the sensitivity of peripheral GRs in antidepressant-resistant major depressives and investigate the association between GR sensitivity and circulating plasma cytokines.Method. Nineteen antidepressant-resistant depressives together with age- and sex-matched healthy controls underwent the steroid vasoconstriction assay using three commercial preparations of corticosteroids containing clobetasol propionate 0·05%, betamethasone valerate 0·1%, and clobetasone butyrate 0·05%, corresponding to very potent, potent, and moderately potent steroid creams respectively. The pro-inflammatory cytokines, tumour necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) were measured using enzyme-linked immunosorbent assays. The severity of the depressive episode was assessed using the Hamilton Depression Scale (HAMD).Results. Depressed subjects had a significantly reduced vasoconstriction response across all three strengths of steroid. They also had significantly higher concentrations of TNF-α and IL-6. There was a significant inverse correlation between TNF-α concentration and vasoconstriction response and also between the HAMD score and vasoconstriction response.Conclusions. These findings suggest that cutaneous GR function is abnormal in antidepressant-resistant depression, that circulating TNF-α may play a significant role in this abnormality and that the efficacy of topical steroids in antidepressant-resistant depressives is reduced.
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Chakkarwar, Prashant Ramesh. "Montelukast - Its Immunomodulatory and Antiviral Action in COVID-19." Journal of Evidence Based Medicine and Healthcare 8, no. 21 (May 24, 2021): 1731–32. http://dx.doi.org/10.18410/jebmh/2021/327.
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Coronavirus disease-19 (COVID-19) is the deadliest pandemic that the whole world is facing today. COVID-19 is different from normal flu by its two lethal manifestations which includes deadly pneumonia which may lead to acute respiratory distress syndrome (ARDS) due to hyper-inflammation of alveolar tissues and pulmonary intravascular coagulopathy (PIC).1,2 It is noteworthy here to mention that both these lethal manifestations of COVID-19 are due to abnormally high levels of pro-inflammatory cytokines like interleukin (IL) - 1β, IL - 6, and tumour necrosis factor (TNF) - α, termed as “cytokine storm.”3,4 There is a certain link between pro-inflammatory cytokines like IL - 1β, IL - 6, and TNF - α and its pro-coagulatory influence on coagulation pathway mediated by tissue factor that binds and activate factor VII, leading to formation of tissue factor – VII a complexes which results in the activation of clotting factor X and IX.4 Recently the researchers in China and some European countries have found raised level of pro-inflammatory cytokines particularly IL - 6 in severe cases of COVID-19. They also found raised D-dimer, fibrinogen levels and prothrombin time in moderate to severe COVID-19 cases.5,6 Both of these lethal manifestations of COVID-19 – ARDS and PIC are linked to raised levels of pro-inflammatory cytokines, particularly, IL - 6. It is not very clear that the pro-inflammatory action of cytokines is mediated through leukotrienes as the biochemical assay for leukotrienes are not widely available but possibility of this probable mechanism cannot be ruled out. Hence, development of any molecule with ability to inhibit pro-inflammatory cytokines, particularly IL-6 may be able to tame the lethal nature of COVID-19, and may ultimately reduce the mortality of this deadly pandemic. Montelukast sodium is such molecule which has capacity to inhibit proinflammatory cytokines such as IL - 1β, IL - 6, and TNF - α.7 Montelukast sodium is leukotriene receptor antagonist that inhibits the cysteinyl leukotriene type-1 receptor. Leukotrienes modulate the production of pro-inflammatory cytokines.8 Its antagonist action on leukotriene receptors can inhibit the production of these pro-inflammatory cytokines. Even recent in silico study by Jacobson at Oak Ridge National Lab, was found that excess bradykinin production may be responsible for pulmonary, cardiac, neurological and nephrological lethal manifestations of COVID-19.9 Crimi et al.10 already found that Montelukast is effective to control bradykinin induced bronchoconstriction. Thus, theoretically, montelukast seems to be best molecule to deal with deadly manifestation of COVID-19 even if we go by cytokine storm hypothesis or bradykinin hypothesis.