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Condition: Inflammatory Bowel Disease

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Total 147 results found since Jan 2013.

Increased Expression of Interleukin-36, a Member of the Interleukin-1 Cytokine Family, in Inflammatory Bowel Disease
Conclusions: IL-36α and IL-36γ may play a proinflammatory role in the pathophysiology of inflammatory bowel disease through induction of CXC chemokines and acute phase proteins.
Source: Inflammatory Bowel Diseases - January 24, 2016 Category: Gastroenterology Tags: Original Basic Science Articles Source Type: research

De Novo sphingolipid synthesis is essential for Salmonella -induced autophagy and human beta-defensin 2 expression in intestinal epithelial cells
Conclusions Our results offer mechanistic insights on the role of de novo sphingolipid synthesis in the innate immunity of intestinal epithelial cells to Salmonella infection. The pharmaceuticals enhancing or diet enriched with sphingolipids may induce the dual anti-bacterial mechanisms. The role of de novo sphingolipid synthesis on inflammatory bowel disease is deserved to be further investigated.
Source: Gut Pathogens - February 18, 2016 Category: Microbiology Source Type: research

Oroxyloside prevents dextran sulfate sodium-induced experimental colitis in mice by inhibiting NF-κB pathway through PPARγ activation.
Abstract Oroxyloside, as a metabolite of oroxylin A, may harbor various beneficial bioactivities which have rarely been reported in the previous studies. Here we established the dextran sulfate sodium (DSS)-induced experimental colitis and evaluated the anti-inflammatory effect of oroxyloside in vivo. As a result, oroxyloside attenuated DSS-induced body weight loss, colon length shortening and colonic pathological damage. Furthermore, oroxyloside inhibited inflammatory cells infiltration and decreased myeloperoxidase (MPO) and inducible nitric oxide synthase (iNOS) activities as well. The production of pro-inflamm...
Source: Biochemical Pharmacology - March 3, 2016 Category: Drugs & Pharmacology Authors: Wang X, Sun Y, Zhao Y, Ding Y, Zhang X, Kong L, Li Z, Guo Q, Zhao L Tags: Biochem Pharmacol Source Type: research

Ulcerative Colitis-Associated Long Noncoding RNA, BC012900, Regulates Intestinal Epithelial Cell Apoptosis
Conclusions: Multiple lncRNAs are differentially expressed in IBD and play a role in regulating cellular physiology. Our results indicate that lncRNAs may be integral modulators of intestinal inflammation associated with IBD and represent novel targets for future therapeutics and diagnostic marker development.
Source: Inflammatory Bowel Diseases - March 15, 2016 Category: Gastroenterology Tags: Original Basic Science Articles Source Type: research

The suppressor of cytokine signaling SOCS1 promotes apoptosis of intestinal epithelial cells via p53 signaling in Crohn's Disease.
This study was designed to investigate whether SOCS1 has a role in the death of intestinal epithelial cells and intestinal injury. The results showed that the expression of SOCS1 increased in CD patients, and the expression of SOCS1, p-p53 and PUMA increased in mouse TNBS induced colitis model. Using IFN-γ treated HT-29 cells as an apoptotic model of intestinal epithelial cells in vitro, we confirmed that SOCS1 promoted apoptosis of intestinal epithelial cells by activating p53. In HT-29 cells which were treated with IFN-γ, the interaction between p53 and SOCS1 and phosphorylation of p53 was significantly higher than unt...
Source: Experimental and Molecular Pathology - May 24, 2016 Category: Pathology Authors: Cui X, Shan X, Qian J, Ji Q, Wang L, Wang X, Li M, Ding H, Liu Q, Chen L, Zhang D, Ni R Tags: Exp Mol Pathol Source Type: research

GSE69445 Crohn's disease risk variant in GPR65 alters lysosomal function
Contributors : K Lassen ; G Goel ; R J XavierSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusUsing an siRNA screen we identify a role for GPR65 in the defense against intracellular pathogens. Epithelial cells and macrophages lacking GPR65 exhibited impaired clearance of intracellular bacteria as well as an accumulation of aberrant phagosomes and lysosomes. Transcriptional profiling revealed changes in genes associated with lysosomal function.
Source: GEO: Gene Expression Omnibus - June 15, 2016 Category: Genetics & Stem Cells Tags: Expression profiling by high throughput sequencing Mus musculus Source Type: research

Hydrogen sulfide improves colonic barrier integrity in DSS-induced inflammation in Caco-2 cells and mice.
In conclusion, endogenous H2S system involves in DSS-induced inflammation and H2S addition alleviated inflammation and intestinal dysfunction in vitro and in vivo. PMID: 27472293 [PubMed - as supplied by publisher]
Source: International Immunopharmacology - July 25, 2016 Category: Allergy & Immunology Authors: Zhao H, Yan R, Zhou X, Ji F, Zhang B Tags: Int Immunopharmacol Source Type: research

The serine protease-mediated increase in intestinal epithelial barrier function is dependent on occludin and requires an intact tight junction.
Abstract Barrier dysfunction is a characteristic of the inflammatory bowel diseases (IBD), Crohn's disease and ulcerative colitis. Understanding how the tight junction is modified to maintain barrier function may provide avenues for treatment of IBD. We have previously shown that the apical addition of serine proteases to intestinal epithelial cell lines causes a rapid and sustained increase in transepithelial electrical resistance (TER), but the mechanisms are unknown. We hypothesized that serine proteases increase barrier function through trafficking and insertion of tight junction proteins into the membrane, an...
Source: American Journal of Physiology. Gastrointestinal and Liver Physiology - August 3, 2016 Category: Physiology Authors: Ronaghan NJ, Shang J, Iablokov V, Zaheer R, Colarusso P, Turner JR, MacNaughton WK Tags: Am J Physiol Gastrointest Liver Physiol Source Type: research

The serine protease-mediated increase in intestinal epithelial barrier function is dependent on occludin and requires an intact tight junction
Barrier dysfunction is a characteristic of the inflammatory bowel diseases (IBD), Crohn's disease and ulcerative colitis. Understanding how the tight junction is modified to maintain barrier function may provide avenues for treatment of IBD. We have previously shown that the apical addition of serine proteases to intestinal epithelial cell lines causes a rapid and sustained increase in transepithelial electrical resistance (TER), but the mechanisms are unknown. We hypothesized that serine proteases increase barrier function through trafficking and insertion of tight junction proteins into the membrane, and this could enhan...
Source: AJP: Gastrointestinal and Liver Physiology - August 31, 2016 Category: Gastroenterology Authors: Ronaghan, N. J., Shang, J., Iablokov, V., Zaheer, R., Colarusso, P., Turner, J. R., MacNaughton, W. K. Tags: EPITHELIAL BIOLOGY AND SECRETION Source Type: research

Differential effects of {alpha}4{beta}7 and GPR15 on homing of effector and regulatory T cells from patients with UC to the inflamed gut in vivo
Conclusions α4β7 rather than GPR15 is crucial for increased colonic homing of UC Treg cells in vivo, while both receptors control UC Teff cell homing. Vedolizumab treatment impairs homing of UC Treg cells leading to their accumulation in peripheral blood with subsequent suppression of systemic Teff cell expansion.
Source: Gut - September 7, 2016 Category: Gastroenterology Authors: Fischer, A., Zundler, S., Atreya, R., Rath, T., Voskens, C., Hirschmann, S., Lopez-Posadas, R., Watson, A., Becker, C., Schuler, G., Neufert, C., Atreya, I., Neurath, M. F. Tags: Open access Inflammatory bowel disease Source Type: research

MicroRNA-206 is involved in the pathogenesis of ulcerative colitis via regulation of adenosine A3 receptor.
Authors: Wu W, He Y, Feng X, Ye S, Wang H, Tan W, Yu C, Hu J, Zheng R, Zhou Y Abstract Increasing evidence suggests that miRNAs are widely dysregulated in ulcerative colitis (UC), potentially affecting UC pathogenesis, diagnosis, and therapy. microRNA (miR) -206 has been reported to be upregulated in UC; however, its function and role in UC remain unknown. Here, we elucidate the function of miR-206 in the pathogenesis of UC. In patients with active-UC, miR-206 and adenosine A3 receptor (A3AR) levels were significantly upregulated and downregulated, respectively, and were inversely correlated. A3AR was expressed in ...
Source: Oncotarget - November 29, 2016 Category: Cancer & Oncology Tags: Oncotarget Source Type: research

GPR4 deficiency alleviates intestinal inflammation in a mouse model of acute experimental colitis
Publication date: February 2017 Source:Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, Volume 1863, Issue 2 Author(s): Edward J. Sanderlin, Nancy R. Leffler, Kvin Lertpiriyapong, Qi Cai, Heng Hong, Vasudevan Bakthavatchalu, James G. Fox, Joani Zary Oswald, Calvin R. Justus, Elizabeth A. Krewson, Dorcas O’Rourke, Li V. Yang GPR4 is a proton-sensing G protein-coupled receptor that can be activated by extracellular acidosis. It has recently been demonstrated that activation of GPR4 by acidosis increases the expression of numerous inflammatory and stress response genes in vascular endothelial cells (ECs) a...
Source: Biochimica et Biophysica Acta (BBA) Molecular Basis of Disease - December 11, 2016 Category: Molecular Biology Source Type: research

miRNA-133a-UCP2 pathway regulates inflammatory bowel disease progress by influencing inflammation, oxidative stress and energy metabolism.
CONCLUSION: The miR-133a-UCP2 pathway participates in IBD by altering downstream inflammation, oxidative stress and markers of energy metabolism, which provides novel clues and potential therapeutic targets for IBD. PMID: 28104982 [PubMed - in process]
Source: World Journal of Gastroenterology : WJG - January 6, 2017 Category: Gastroenterology Authors: Jin X, Chen D, Zheng RH, Zhang H, Chen YP, Xiang Z Tags: World J Gastroenterol Source Type: research

GWAS for serum galactose-deficient IgA1 implicates critical genes of the < i > O < /i > -glycosylation pathway
by Krzysztof Kiryluk, Yifu Li, Zina Moldoveanu, Hitoshi Suzuki, Colin Reily, Ping Hou, Jingyuan Xie, Nikol Mladkova, Sindhuri Prakash, Clara Fischman, Samantha Shapiro, Robert A. LeDesma, Drew Bradbury, Iuliana Ionita-Laza, Frank Eitner, Thomas Rauen, Nicolas Maillard, Francois Berthoux, J ürgen Floege, Nan Chen, Hong Zhang, Francesco Scolari, Robert J. Wyatt, Bruce A. Julian, Ali G. Gharavi, Jan Novak AberrantO-glycosylation of serum immunoglobulin A1 (IgA1) represents a heritable pathogenic defect in IgA nephropathy, the most common form of glomerulonephritis worldwide, but specific genetic factors involved in its dete...
Source: PLoS Genetics - February 9, 2017 Category: Genetics & Stem Cells Authors: Krzysztof Kiryluk Source Type: research

Microtubule-associated protein 1S-related autophagy inhibits apoptosis of intestinal epithelial cells via Wnt/ β-catenin signaling in Crohn's disease.
Microtubule-associated protein 1S-related autophagy inhibits apoptosis of intestinal epithelial cells via Wnt/β-catenin signaling in Crohn's disease. Biochem Biophys Res Commun. 2017 Feb 07;: Authors: Bai W, Bai J, Li Y, Tian D, Shi R Abstract Many autophagy-related genes, to our knowledge, have been identified as Crohn's disease (CD) polymorphic sites by genomic wide studies. As a novel member of the microtubule-associated protein 1 (MAP1) family, MAP1S is a microtubule-binding proteins involved in autophagy. However, its expression and potential functions in CD have not been understood. For the fir...
Source: Biochemical and Biophysical Research communications - February 6, 2017 Category: Biochemistry Authors: Bai W, Bai J, Li Y, Tian D, Shi R Tags: Biochem Biophys Res Commun Source Type: research