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Condition: Inflammatory Bowel Disease

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Total 147 results found since Jan 2013.

1,25 ‑Dihydroxyvitamin D regulates macrophage polarization and ameliorates experimental inflammatory bowel disease by suppressing miR-125b.
This study aimed to explore whether 1,25(OH)2D3 modulates macrophage polarization in inflammation. Peripheral blood mononuclear cells and colitis mice were treated with 1,25(OH)2D3. Macrophages were transfected with siRNA-vitamin D receptor (VDR) or miR-125b mimic or inhibitor, and 1,25(OH)2D3-pretreated colitis mice were injected with a miR-125b agomir. The distribution of macrophage subsets and macrophage subtype characteristics was analyzed. As expected, 1,25(OH)2D3 transformed lipopolysaccharide-induced M1 macrophages to the M2 subset, downregulated tumor necrosis factor-α and interleukin (IL)-6 expression and interfe...
Source: International Immunopharmacology - December 9, 2018 Category: Allergy & Immunology Authors: Zhu X, Zhu Y, Li C, Yu J, Ren D, Qiu S, Nie Y, Yu X, Xu X, Zhu W Tags: Int Immunopharmacol Source Type: research

EZH2 Regulates Intestinal Inflammation and Necroptosis Through the JNK Signaling Pathway in Intestinal Epithelial Cells
ConclusionOur data suggest that EZH2 plays an important role in the development of intestinal inflammation and necroptosis. Hence, EZH2 could be a potential therapeutic target for IBD.
Source: Digestive Diseases and Sciences - July 3, 2019 Category: Gastroenterology Source Type: research

lncRNA Mirt2 Is Downregulated in Ulcerative Colitis and Regulates IL-22 Expression and Apoptosis in Colonic Epithelial Cells.
Authors: Ding G, Ming Y, Zhang Y Abstract lncRNA Mirt2 is a lipopolysaccharide- (LPS-) inducible inflammation inhibitor. We found that Mirt2 was downregulated in plasma of ulcerative colitis (UC) patients and the downregulation of Mirt2 distinguished UC patients from healthy controls. IL-22 was also downregulated in UC patients and positively correlated with Mirt2. Mirt2 overexpression led to upregulated, while Mirt2 siRNA silencing led to inhibited secretion of IL-22 from colonic epithelial cells treated with LPS. In addition, under LPS treatment, Mirt2 overexpression led to decreased, while Mirt2 siRNA silencing ...
Source: Gastroenterology Research and Practice - November 8, 2019 Category: Gastroenterology Tags: Gastroenterol Res Pract Source Type: research

Autotaxin stimulates LPA2 receptor in macrophages and exacerbates dextran sulfate sodium-induced acute colitis
AbstractAutotaxin (ATX) is a secreted enzyme that hydrolyzes lysophosphatidylcholine (LPC) to lysophosphatidic acid (LPA) and choline. ATX has been implicated in multiple chronic inflammatory diseases, but little is known about its role in the development of inflammatory bowel disease (IBD). Here, we investigated how ATX contributed to intestinal inflammation during colitis. We found that ATX expression levels were upregulated in the intestines of ulcerative colitis (UC) patients in acute state as well as in the intestines of dextran sulfate sodium (DSS)-induced colitis mice, which is likely due to increased infiltration o...
Source: Journal of Molecular Medicine - October 31, 2020 Category: Molecular Biology Source Type: research

CYP24A1 Involvement in Inflammatory Factor Regulation Occurs via the Wnt Signaling Pathway
ConclusionTaken together, this study suggests that inflammatory factors may increase CYP24A1 expressionvia NF- κB pathway activation, which in turn stimulates Wnt signaling.
Source: Journal of Huazhong University of Science and Technology -- Medical Sciences -- - October 17, 2022 Category: Research Source Type: research

Research Resource A Genome-Wide siRNA Screen Reveals Positive and Negative Regulators of the NOD2 and NF-{kappa}B Signaling Pathways
A small interfering RNA screen provides insight into the mechanisms of Crohn's disease pathogenesis.
Source: Signal Transduction Knowledge Environment - January 16, 2013 Category: Science Authors: Neil Warner, Aaron Burberry, Luigi Franchi, Yun-Gi Kim, Christine McDonald, Maureen A. Sartor, Gabriel Nunez Source Type: news

Novel transcriptional regulation of VEGF in inflammatory processes.
This study builds upon our previous results in testing the role of mouse LITAF and STAT6B in the regulation of VEGF-mediated processes. Cells cotransfected with a series of VEGF promoter deletions along with truncated forms of mLITAF and/or mSTAT6B identified a DNA binding site (between -338 and -305 upstream of the transcription site) important in LITAF and/or STAT6B-mediated transcriptional regulation of VEGF. LITAF and STAT6B corresponding protein sites were identified. In addition, siRNA-mediated knockdown of mLITAF and/or mSTAT6B leads to significant reduction in VEGF mRNA levels and inhibits LPS-induced VEGF secretio...
Source: J Cell Mol Med - February 18, 2013 Category: Molecular Biology Authors: Tang X, Yang Y, Yuan H, You J, Burkatovskaya M, Amar S Tags: J Cell Mol Med Source Type: research

Death-Associated Protein Kinase Controls STAT3 Activity in Intestinal Epithelial Cells.
ider-Stock R Abstract The TNF-IL-6-STAT3 pathway plays a crucial role in promoting ulcerative colitis-associated carcinoma (UCC). To date, the negative regulation of STAT3 is poorly understood. Interestingly, intestinal epithelial cells of UCC in comparison to ulcerative colitis show high expression levels of anti-inflammatory death-associated protein kinase (DAPK) and low levels of pSTAT3. Accordingly, epithelial DAPK expression was enhanced in STAT3(IEC-KO) mice. To unravel a possible regulatory mechanism, we used an in vitro TNF-treated intestinal epithelial cell model. We identified a new function of DAPK in ...
Source: The American Journal of Pathology - March 1, 2013 Category: Pathology Authors: Chakilam S, Gandesiri M, Rau TT, Agaimy A, Vijayalakshmi M, Ivanovska J, Wirtz RM, Schulze-Luehrmann J, Benderska N, Wittkopf N, Chellappan A, Ruemmele P, Vieth M, Rave-Fränk M, Christiansen H, Hartmann A, Neufert C, Atreya R, Becker C, Steinberg P, Schn Tags: Am J Pathol Source Type: research

Multiple activating and repressive cis-promoter regions regulate TNFSF15 expression in human primary mononuclear cells.
Abstract TL1A/TNFSF15 has been associated with IBD (inflammatory bowel disease) in GWAS (genome-wide association study) and plays a role mediating mucosal inflammation in IBD. Higher TL1A expression is associated with disease severity in both patients and mouse models. Although TL1A has been studied extensively for IBD-associated SNPs, the cis/trans-regulatory regions are poorly defined. Herein we identify response elements regulating TNFSF15 in primary human myeloid cells. Peripheral mononuclear cells transfected with TNFSF15 promoter constructs displayed 30-fold enhanced promoter activity in a minimal -74bp regi...
Source: Cytokine - April 30, 2013 Category: Molecular Biology Authors: Gonsky R, Deem RL, Targan SR Tags: Cytokine Source Type: research

Impaired autophagy leads to abnormal dendritic cell–epithelial cell interactions
Conclusions: In intestinal DC–epithelial cell interactions, autophagy deficiency leads to decreased antigen sampling, increased DC maturation and a more pro-inflammatory type of DC.
Source: Journal of Critical Care - September 17, 2012 Category: Gastroenterology Authors: Caterina Strisciuglio, Marjolijn Duijvestein, Auke P. Verhaar, Anne Christine W. Vos, Gijs R. van den Brink, Daniel W. Hommes, Manon E. Wildenberg Tags: Regular papers Source Type: research

The cysteinyl leukotriene 2 receptor contributes to all-trans retinoic acid-induced differentiation of colon cancer cells
Conclusions: This study identifies a novel mechanism of action for ATRA in colorectal cancer cell differentiation and demonstrates that retinoids can have anti-tumorigenic effects through their action on the cysteinyl leukotriene pathway.
Source: BMC Cancer - July 8, 2013 Category: Cancer & Oncology Authors: Astrid BengtssonGunilla JönssonCecilia MagnussonTavga SalimCecilia AxelssonAnita Sjölander Source Type: research

Serotonin regulates innate immune responses of colon epithelial cells through NOX2-derived reactive oxygen species.
In this study, we examined the role and mechanism of action of 5-HT in inflammatory response of colon epithelial cells in vitro and in vivo. In colon epithelial cells (CCD 841, HT-29, Caco-2), direct application of 5-HT induced production of ROS and monocyte-epithelial adhesion, an initial event of inflammation, which were blocked not only by 5-HT receptor antagonists (tropisetron, RS39604, and SB269970), antioxidants (ascorbic acid, apocynin) and various inhibitors of NADPH oxidase (DPI), CREB (KG-501), and NF-κB (PDTC), but also by transfection with Nox2 siRNA. Nox2-derived production of ROS corresponded with the rapid ...
Source: Free Radical Biology and Medicine - February 10, 2014 Category: Biology Authors: Chandra Regmi S, Park SY, Kwang Ku S, Kim JA Tags: Free Radic Biol Med Source Type: research

Studies for normal function of prion protein using knockout mice under the immunological or pathophysiological stress
ABSTRACT Deletion of cellular isoform of prion protein (PrPC) increased neuronal predisposition to damage by modulating to apoptosis, and the negative consequences to oxidative stress. In vivo studies demonstrated that PrPC‐deficient mice were more prone to seizure, depression and epilepsy induction, and exhibited an extent of the cerebral damage following an ischemic challenge or viral infection. Besides, adenovirus‐mediated PrPC over‐expression reduces brain damage in rat model of cerebral ischemia. In experimental autoimmune encephalomyelitis (EAE) PrPC‐deficient mice demonstrated more aggressive disease onset a...
Source: Microbiology and Immunology - May 1, 2014 Category: Microbiology Authors: Takashi Onodera, Akikazu Sakudo, Hirokazu Tsubone, Shigeyoshi Itohara Tags: Review Source Type: research

Disruption of macrophage pro-inflammatory cytokine release in Crohn's disease is associated with reduced optineurin expression in a subset of patients.
This article is protected by copyright. All rights reserved. PMID: 24943399 [PubMed - as supplied by publisher]
Source: Immunology - June 18, 2014 Category: Allergy & Immunology Authors: Smith A, Sewell G, Levine A, Chew T, Dunne J, O'Shea N, Smith P, Harrison P, Macdonald C, Bloom S, Segal A Tags: Immunology Source Type: research

Review of studies that have used knockout mice to assess normal function of prion protein under immunological or pathophysiological stress
Abstract Deletion of cellular isoform of prion protein (PrPC) increases neuronal predisposition to damage by modulating apoptosis and the negative consequences of oxidative stress. In vivo studies have demonstrated that PrPC‐deficient mice are more prone to seizure, depression, and induction of epilepsy and experience extensive cerebral damage following ischemic challenge or viral infection. In addition, adenovirus‐mediated overexpression of PrPC reduces brain damage in rat models of cerebral ischemia. In experimental autoimmune encephalomyelitis, PrPC‐deficient mice reportedly have a more aggressive disease onset an...
Source: Microbiology and Immunology - July 8, 2014 Category: Microbiology Authors: Takashi Onodera, Akikazu Sakudo, Hirokazu Tsubone, Shigeyoshi Itohara Tags: Review Source Type: research