scholarly journals TREM-1–expressing intestinal macrophages crucially amplify chronic inflammation in experimental colitis and inflammatory bowel diseases

2007 ◽  
Vol 117 (10) ◽  
pp. 3097-3106 ◽  
Author(s):  
Mirjam Schenk ◽  
Axel Bouchon ◽  
Frank Seibold ◽  
Christoph Mueller
Keyword(s):  
Chronic Inflammation ◽  
Inflammatory Bowel Diseases ◽  
Experimental Colitis ◽  
Bowel Diseases ◽  
Inflammatory Bowel

GLUT5 is a determinant of dietary fructose-mediated exacerbation of experimental colitis

2021 ◽  
Author(s):  
Srijani Basu ◽  
Catherine Liu ◽  
Xi Kathy Zhou ◽  
Ryohei Nishiguchi ◽  
Taehoon Ha ◽  
...  
Keyword(s):  
Inflammatory Bowel Diseases ◽  
Experimental Colitis ◽  
Fecal Microbiota ◽  
Genetically Engineered ◽  
Western Diet ◽  
High Fructose ◽  
Genetically Engineered Mice ◽  
Dietary Fructose ◽  
Bowel Diseases ◽  
Inflammatory Bowel

The western diet has been suggested to contribute to the rising incidence of Inflammatory Bowel Diseases. This has led to the hypothesis that fructose, a component of the western diet, could play a role in the pathogenesis of Inflammatory Bowel Diseases. A high fructose diet is known to exacerbate experimental colitis. This study tested whether the expression of GLUT5, the fructose transporter, is a determinant of the severity of experimental colitis during elevated fructose consumption and whether ileal inflammation is associated with altered GLUT5 expression in Crohn's Disease. Studies in genetically engineered mice showed that in comparison to Glut5+/+ mice, feeding a 15 kcal% fructose diet to Glut5-/- mice led to worse dextran sodium sulfate (DSS)-induced colitis. This effect was associated with elevated levels of colonic fructose and a shift in the fecal microbiota in Glut5-/- mice. Importantly, treatment with broad-spectrum antibiotics protected against the worsening of colitis mediated by dietary fructose in Glut5-/- mice. Gene expression analysis revealed that GLUT5 levels are reduced in patients with Crohn's ileitis. Moreover, levels of GLUT5 negatively correlated with levels of pro-inflammatory mediators. Collectively, these results demonstrate that dietary constituent (fructose)-host gene (GLUT5) interactions can shape the colonic microbiota thereby impacting the severity of colitis.

Accurate and rapid microfluidic ELISA to monitor Infliximab titers in patients with inflammatory bowel diseases

The Analyst ◽  
2022 ◽  
Author(s):  
Inês Iria ◽  
Ruben R.G. Soares ◽  
Eduardo Brás ◽  
Virginia Chu ◽  
João Gonçalves ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Gastrointestinal Tract ◽  
Chronic Inflammation ◽  
Inflammatory Bowel Diseases ◽  
Bowel Disease ◽  
Biological Therapy ◽  
Bowel Diseases ◽  
Inflammatory Bowel

Inflammatory bowel disease (IBD) is a term used to describe disorders that involve chronic inflammation in the gastrointestinal tract, affecting more than 6.8 million people worldwide.1 Biological therapy is used...

scholarly journals Distinct roles of intracellular heat shock protein 70 in maintaining gastrointestinal homeostasis

2018 ◽  
Vol 314 (2) ◽  
pp. G164-G178 ◽  
Author(s):  
Yunwei Wang ◽  
Fanfei Lin ◽  
Xiaorong Zhu ◽  
Vanessa A. Leone ◽  
Sushila Dalal ◽  
...  
Keyword(s):  
Heat Shock ◽  
Heat Shock Protein ◽  
Immune Regulation ◽  
Inflammatory Bowel Diseases ◽  
Heat Shock Protein 70 ◽  
Experimental Colitis ◽  
Cell Types ◽  
Bowel Diseases ◽  
Inflammatory Bowel ◽  
Chronic Intestinal Inflammation

The inducible heat shock protein 70 (Hsp70) is both cytoprotective and immunomodulatory, potentially accounting for its critical role in maintaining gastrointestinal homeostasis. When levels are reduced in conditions like inflammatory bowel diseases (IBD), loss of function contributes to the severity and chronicity of these diseases, although through which cell types and mechanisms remains unclear. Here, the role of Hsp70-mediated intestinal epithelial protection and immune regulation in experimental colitis was examined by using a villin promoter-driven Hsp70 transgene in the 2,4,6-trinitrobenzene sulfonic acid (TNBS) and dextran sodium sulfate (DSS) models and in IL-10/Hsp70 double knockout (IL10−/−/Hsp70−/−) mice. In addition, Hsp70-mediated IL-10 production and immune protection were investigated using a CD45RBhigh transfer model and measuring colonic and immune cell cytokine expression during colitis. We found that the epithelial-specific expression of Hsp70 transgene attenuated DSS-induced colitis in Hsp70−/− mice by protecting tight junctions (TJ) and their interaction with the TJ-associated protein ZO-1. In the TNBS colitis and CD45RBhigh model, Hsp70 carried out its intracellular anti-inflammatory function by maintaining IL-10 production. Impaired ERK phosphorylation, but not p38 or JNK phosphorylation pathways, was associated with decreased IL-10 production in Hsp70-deficient cells. Together, these actions can be leveraged in the context of cellular specificity to develop complementary strategies that can lead to reduction in mucosal injury and immune activation in colonic colitis development. NEW & NOTEWORTHY Using four different experimental colitis models, we filled an important gap in knowledge by defining essential roles of intracellular heat shock protein 70 in different cell types in maintaining intestinal integrity and immune regulation. These findings are relevant to human inflammatory bowel diseases and represent potential avenues for developing therapeutic strategies, not only to counter the destructive processes of inflammation but also to promote tissue healing and prevent complications frequently associated with chronic intestinal inflammation.

Orally available extract from Brassica oleracea var. capitata rubra attenuates experimental colitis in mouse models of inflammatory bowel diseases

2015 ◽  
Vol 17 ◽  
pp. 587-599 ◽  
Author(s):  
Marta Zielińska ◽  
Urszula Lewandowska ◽  
Anna Podsędek ◽  
Adam I. Cygankiewicz ◽  
Damian Jacenik ◽  
...  
Keyword(s):  
Brassica Oleracea ◽  
Mouse Models ◽  
Inflammatory Bowel Diseases ◽  
Experimental Colitis ◽  
Bowel Diseases ◽  
Inflammatory Bowel
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