Caffeic acid attenuates 12-O-tetradecanoyl-phorbol-13-acetate (TPA)-induced NF-κB and COX-2 expression in mouse skin: Abrogation of oxidative stress, inflammatory responses and proinflammatory cytokine production

2012 ◽  
Vol 50 (2) ◽  
pp. 175-183 ◽  
Author(s):  
Abdul Quaiyoom Khan ◽  
Rehan Khan ◽  
Wajhul Qamar ◽  
Abdul Lateef ◽  
Farrah Ali ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Caffeic Acid ◽  
Proinflammatory Cytokine ◽  
Cytokine Production ◽  
Inflammatory Responses ◽  
Mouse Skin ◽  
Proinflammatory Cytokine Production ◽  
Cox 2

scholarly journals Oxidative Stress and Inflammation: Essential Partners in Alcoholic Liver Disease

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Aditya Ambade ◽  
Pranoti Mandrekar
Keyword(s):  
Oxidative Stress ◽  
Liver Disease ◽  
Alcoholic Liver Disease ◽  
Cytokine Production ◽  
Inflammatory Responses ◽  
Proinflammatory Cytokine Production ◽  
The Past ◽  
Proinflammatory Responses ◽  
Progression Of Disease ◽  
Oxidative Processes

Alcoholic liver disease (ALD) is a multifaceted disease that is characterized by hepatic steatosis or fat deposition and hepatitis or inflammation. Over the past decade, multiple lines of evidence have emerged on the mechanisms associated with ALD. The key mechanisms identified so far are sensitization to gut-derived endotoxin/lipopolysaccharide resulting in proinflammatory cytokine production and cellular stress due to oxidative processes, contributing to the development and progression of disease. While oxidative stress and inflammatory responses are studied independently in ALD, mechanisms linking these two processes play a major role in pathogenesis of disease. Here we review major players of oxidative stress and inflammation and highlight signaling intermediates regulated by oxidative stress that provokes proinflammatory responses in alcoholic liver disease.

Soluble uric acid primes TLR-induced proinflammatory cytokine production by human primary cells via inhibition of IL-1Ra

2015 ◽  
Vol 75 (4) ◽  
pp. 755-762 ◽  
Author(s):  
Tania O Crișan ◽  
Maartje C P Cleophas ◽  
Marije Oosting ◽  
Heidi Lemmers ◽  
Helga Toenhake-Dijkstra ◽  
...  
Keyword(s):  
Uric Acid ◽  
Histone Methylation ◽  
Proinflammatory Cytokine ◽  
Mononuclear Cells ◽  
Cytokine Production ◽  
Inflammatory Responses ◽  
Soluble Form ◽  
Mrna Levels ◽  
Proinflammatory Cytokine Production ◽  
Msu Crystals

ObjectivesThe study of the proinflammatory role of uric acid has focused on the effects of its crystals of monosodium urate (MSU). However, little is known whether uric acid itself can directly have proinflammatory effects. In this study, we investigate the priming effects of uric acid exposure on the cytokine production of primary human cells upon stimulation with gout-related stimuli.MethodsPeripheral blood mononuclear cells (PBMCs) were harvested from patients with gout and healthy volunteers. Cells were pretreated with or without uric acid in soluble form for 24 h and then stimulated for 24 h with toll-like receptor (TLR)2 or TLR4 ligands in the presence or absence of MSU crystals. Cytokine production was measured by ELISA; mRNA levels were assessed using qPCR.ResultsThe production of interleukin (IL)-1β and IL-6 was higher in patients compared with controls and this correlated with serum urate levels. Proinflammatory cytokine production was significantly potentiated when cells from healthy subjects were pretreated with uric acid. Surprisingly, this was associated with a significant downregulation of the anti-inflammatory cytokine IL-1 receptor antagonist (IL-1Ra). This effect was specific to stimulation by uric acid and was exerted at the level of gene transcription. Epigenetic reprogramming at the level of histone methylation by uric acid was involved in this effect.ConclusionsIn this study we demonstrate a mechanism through which high concentrations of uric acid (up to 50 mg/dL) influence inflammatory responses by facilitating IL-1β production in PBMCs. We show that a mechanism for the amplification of IL-1β consists in the downregulation of IL-1Ra and that this effect could be exerted via epigenetic mechanisms such as histone methylation. Hyperuricaemia causes a shift in the IL-1β/IL-1Ra balance produced by PBMCs after exposure to MSU crystals and TLR-mediated stimuli, and this phenomenon is likely to reinforce the enhanced state of chronic inflammation.

scholarly journals Mitochondrial reactive oxygen species drive proinflammatory cytokine production

2011 ◽  
Vol 208 (3) ◽  
pp. 417-420 ◽  
Author(s):  
Edwina Naik ◽  
Vishva M. Dixit
Keyword(s):  
Reactive Oxygen Species ◽  
Proinflammatory Cytokine ◽  
Inflammatory Cytokine ◽  
Cytokine Production ◽  
Inflammatory Responses ◽  
Reactive Oxygen ◽  
Molecular Pathways ◽  
Oxygen Species ◽  
Proinflammatory Cytokine Production ◽  
Mitochondrial Reactive Oxygen Species

High levels of reactive oxygen species (ROS) are observed in chronic human diseases such as neurodegeneration, Crohn’s disease, and cancer. In addition to the presence of oxidative stress, these diseases are also characterized by deregulated inflammatory responses, including but not limited to proinflammatory cytokine production. New work exploring the mechanisms linking ROS and inflammation find that ROS derived from mitochondria act as signal-transducing molecules that provoke the up-regulation of inflammatory cytokine subsets via distinct molecular pathways.

scholarly journals Berberine promotes recovery of colitis and inhibits inflammatory responses in colonic macrophages and epithelial cells in DSS-treated mice

2012 ◽  
Vol 302 (5) ◽  
pp. G504-G514 ◽  
Author(s):  
Fang Yan ◽  
Lihong Wang ◽  
Yan Shi ◽  
Hanwei Cao ◽  
Liping Liu ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Signaling Pathways ◽  
Proinflammatory Cytokine ◽  
Cytokine Production ◽  
Inflammatory Responses ◽  
Body Weight Loss ◽  
Intestinal Injury ◽  
Myeloperoxidase Activity ◽  
Proinflammatory Cytokine Production ◽  
Beneficial Effects

Inflammatory bowel disease (IBD) results from dysregulation of intestinal mucosal immune responses to microflora in genetically susceptible hosts. A major challenge for IBD research is to develop new strategies for treating this disease. Berberine, an alkaloid derived from plants, is an alternative medicine for treating bacterial diarrhea and intestinal parasite infections. Recent studies suggest that berberine exerts several other beneficial effects, including inducing anti-inflammatory responses. This study determined the effect of berberine on treating dextran sulfate sodium (DSS)-induced intestinal injury and colitis in mice. Berberine was administered through gavage to mice with established DSS-induced intestinal injury and colitis. Clinical parameters, intestinal integrity, proinflammatory cytokine production, and signaling pathways in colonic macrophages and epithelial cells were determined. Berberine ameliorated DSS-induced body weight loss, myeloperoxidase activity, shortening of the colon, injury, and inflammation scores. DSS-upregulated proinflammatory cytokine levels in the colon, including TNF, IFN-γ, KC, and IL-17 were reduced by berberine. Berberine decreased DSS-induced disruption of barrier function and apoptosis in the colon epithelium. Furthermore, berberine inhibited proinflammatory cytokine production in colonic macrophages and epithelial cells in DSS-treated mice and promoted apoptosis of colonic macrophages. Activation of signaling pathways involved in stimulation of proinflammatory cytokine production, including MAPK and NF-κB, in colonic macrophages and epithelial cells from DSS-treated mice was decreased by berberine. In summary, berberine promotes recovery of DSS-induced colitis and exerts inhibitory effects on proinflammatory responses in colonic macrophages and epithelial cells. Thus berberine may represent a new therapeutic approach for treating gastrointestinal inflammatory disorders.

scholarly journals Upregulation of TIPE2 attenuates macrophage activation and neuroinflammation after intracerebral hemorrhage in mice

2020 ◽  
Author(s):  
Shudong Liu ◽  
Jie Wang ◽  
Wenyan Li ◽  
Hui Shi ◽  
Changlong Zhou ◽  
...  
Keyword(s):  
Intracerebral Hemorrhage ◽  
Brain Damage ◽  
Proinflammatory Cytokine ◽  
Macrophage Activation ◽  
Cytokine Production ◽  
Inflammatory Responses ◽  
Brain Inflammation ◽  
Negative Regulator ◽  
Proinflammatory Cytokine Production

Abstract Background: Intracerebral hemorrhage (ICH) is a serious disease with high mortality and morbidity, and effective treatment is limited. A large amount of evidence suggests that the inflammatory response contributes to secondary brain damage following ICH. TIPE2 is an essential negative regulator of both innate and adaptive immunity, and depletion of TIPE2 causes inflammatory disease. However, the possible role of TIPE2 following ICH has not been reported. Methods: In this study, we investigated TIPE2 levels and inflammation in macrophages treated with erythrocyte lysate in vitro, and we observed proinflammatory cytokine production, BBB disruption, cerebral water content and neurological damage in ICH mice in vivo. Results: We found that TIPE2 levels were significantly decreased in erythrocyte lysate-treated macrophages compared to control macrophages. Upregulation of TIPE2 decreased macrophage activation and cytokine production and accelerated brain damage in ICH mice. In addition, upregulation of TIPE2 attenuated proinflammatory cytokine production, BBB disruption, and severe brain inflammation after ICH. Conclusion: The results demonstrated that TIPE2 was negatively correlated with the pathogenesis of ICH, which prevented brain injury and attenuated deleterious inflammatory responses following ICH. TIPE2 might serve as a novel target for ICH therapy.

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