colitis/protease

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Cell type-specific mechanisms coupling protease-activated receptor-1 to infectious colitis pathogenesis.

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Protease-activated receptor-1 (PAR-1) plays a major role in multiple disease processes, including colitis. Understanding the mechanisms coupling PAR-1 to disease pathogenesis is complicated by the fact that PAR-1 is broadly expressed across multiple cell

Expression of protease-activated receptor 2 in ulcerative colitis.

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Although tryptase released from mast cells might play a key role in the pathogenesis of ulcerative colitis (UC), the role of protease-activated receptor 2 (PAR2), tryptase receptor, remains unclear in the pathogenesis of this disease. The expressions of PAR2 and tumor necrosis factor (TNF) alpha in

Colonic bacterial proteases to IgA1 and sIgA in patients with ulcerative colitis.

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The colonic faecal and mucosal associated bacterial populations of five patients with ulcerative colitis and four control patients were studied in detail to assess their ability to produce IgA1-proteases. A total of 330 bacterial strains were isolated from the patients with ulcerative colitis and

Effect of T. spiralis Serine protease inhibitors on TNBS-induced experimental colitis mediated by Macrophages.

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Inflammatory bowel disease (IBD) is an autoimmune disease with increasing incidence rate, and divided into ulcerative colitis (UC) and Crohn's disease (CD). And more and more experimental evidence supports that immune disorder is important in the pathogenesis of IBD. Our previous experiments have

The role of up-regulated serine proteases and matrix metalloproteinases in the pathogenesis of a murine model of colitis.

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Proteinases are important at several phases of physiological and pathological inflammation, mediating cellular infiltration, cytokine activation, tissue damage, remodeling, and repair. However, little is known of their role in the pathogenesis of inflammatory bowel disease. The aim of this study was

[Serine protease inhibitors in plasma of patients with ulcerative colitis].

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Serine protease inhibitors (serpins) are the important factors regulating hemostasis and inflammatory mediators activity. The aim of this study was to determine relationships between plasma serine protease inhibitors activities and the course of ulcerative colitis (uc). METHODS 42 patients with uc,

Bcl2L12 mediates effects of protease-activated receptor-2 on the pathogenesis of Th2-dominated responses of patients with ulcerative colitis.

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The immune dysregulation plays an important role in the pathogenesis of ulcerative colitis (UC). Bcl2 like protein-12 (Bcl2L12) and mast cells are involved in immune dysregulation of UC. This study aims to elucidate the role of Bcl2L12 in the contribution to the pathogenesis of T helper (Th)2-biased

Effect of recombinant serine protease from newborn larval stage of Trichinella spiralis on 2,4,6-trinitrobenzene sulfonic acid-induced experimental colitis in mice

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Inflammatory bowel disease (IBD) is a complex immune-mediated disease of gastrointestinal tract that is mainly driven by Th1/Th17 immune response. "Helminth therapy" has emerged, and helminth-derived immunoregulatory molecules are being used as safe and new therapeutic antigens for IBD. Recombinant

Effect of two recombinant Trichinella spiralis serine protease inhibitors on TNBS-induced experimental colitis of mice.

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Inflammatory bowel disease (IBD), which includes ulcerative colitis and Crohn's disease (CD), is a chronic autoimmune disease. Parasitic infections and their products have been shown to have protective effects on autoimmune diseases, including IBD. In this experiment, 96 male BALB/c mice aged 6-8

Protease activity in a hapten-induced model of ulcerative colitis in rats.

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Inflammatory bowel disease (IBD) is a painful and debilitating condition affecting the mucosal lining of the colon and other areas of the gastrointestinal tract. IBD generally falls into two major categories: ulcerative colitis (UC) and Crohn's disease. We have utilized dinitrobenzenesulfonic acid

Treatment of ulcerative colitis with camostat mesilate, a serine protease inhibitor.

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We were able to induce and maintain remission with camostat mesilate, a serine protease inhibitor, in two patients with ulcerative colitis, to whom salicylazosulfapyridine could not be administered due to previous side effects. The enzymatic activity of proteases from granulocyte, pancreatic juice

Serine protease inhibitors protect better than IL-10 and TGF-β anti-inflammatory cytokines against mouse colitis when delivered by recombinant lactococci.

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BACKGROUND Different studies have described the successful use of recombinant lactic acid bacteria (recLAB) to deliver anti-inflammatory molecules at the mucosal level to treat Inflammatory Bowel Disease (IBD). METHODS In order to identify the best strategy to treat IBD using recLAB, we compared the

Intracolonic infusion of fecal supernatants from ulcerative colitis patients triggers altered permeability and inflammation in mice: role of cathepsin G and protease-activated receptor-4.

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BACKGROUND Cathepsin G (Cat-G) is a neutrophil serine-protease found in the colonic lumen of ulcerative colitis (UC) patients. Cat-G is able to activate protease-activated receptor-4 (PAR(4) ) located at the apical side of enterocytes, leading to epithelial barrier disruption. However, the

Promoter methylation of protease-activated receptor (PAR2) is associated with severe clinical phenotypes of ulcerative colitis (UC).

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Tryptase acting at protease-activated receptor 2 (PAR2) contributes to the pathogenesis of Inflammatory bowel diseases (IBDs). DNA methylation has been shown to be an important mechanism in gene silencing. We attempted to clarify the relationship between the promoter methylation of PAR2 and

Effect of recombinant serine protease from adult stage of Trichinella spiralis on TNBS-induced experimental colitis in mice

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Inflammatory bowel disease (IBD), which includes ulcerative colitis (UC) and Crohn's disease (CD), is a chronic autoimmune disease. At present, worms and their products has been shown to have protective effects on immune-mediated diseases. Therefore, we aimed to investigate the effect of the

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