Changes in mucosal fatty acid profile in inflammatory bowel disease and in experimental colitis: a common response to bowel inflammation

Inflammatory bowel disease (IBD), which consists of Crohn's disease (CD) and ulcerative colitis (UC), is a chronic inflammatory disorder of the intestine. The etiology is heterogeneous and multifactorial, including genetic susceptibility, immune-mediated tissue damage, and changes of lumen microenvironment, especially short-chain fatty acid (SCFA) producing bacteria. Several studies reported a decrease in SCFA concentration in both CD and UC. In fact, SCFAs has important roles in accelerating disease remission. This systematic review aimed to evaluate the changes in SCFA concentration, the composition of SCFA-producing bacteria, and SCFA metabolism in IBD. A literature search was conducted via PubMed, Scopus, and CENTRAL by selecting studies according to inclusion and exclusion criteria. The quality and risk of bias assessment were performed using the Newcastle-Ottawa Scale (NOS). Overall, 160 UC and 127 CD patients from 5 studies were reviewed. The SCFA concentration was significantly reduced (p <0.05) in both PC and UC. Moreover, there was a decrease in major SCFA-producing bacteria. Clostridium coccoides were significantly decreased in the feces of active UC (p = 0.015) and CD (p = 0.04). Clostridium leptum was decreased on intestinal mucosal biopsy of active CD and UC (p <0.0001). Faecalibacterium prausnitzii were decreased in active CD faeces (p <0.0001) and UC (p = 0.0001). Butyrate oxidation rate was also reported to decrease in UC compared to control (p<0.0001). In conclusion, the ability of major SCFA-producing bacterial production in IBD was diminished, which implies a decreased protective and anti-inflammatory effect of SCFA that altered its metabolism.

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S1716 A Positive Role of CHOP, a Transcription Factor Involved in ER Stress Response, in Development of Inflammatory Bowel Disease (IBD)-Related Experimental Colitis

Gastroenterology ◽

10.1016/s0016-5085(08)61187-7 ◽

2008 ◽

Vol 134 (4) ◽

pp. A-256

Author(s):

Takushi Namba ◽

Tohru Mizushima

Keyword(s):

Inflammatory Bowel Disease ◽

Transcription Factor ◽

Stress Response ◽

Er Stress ◽

Bowel Disease ◽

Experimental Colitis ◽

Positive Role ◽

Er Stress Response ◽

Inflammatory Bowel

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ErbB-1 experssion in experimental model of inflammatory bowel disease in rats

Acta chirurgica iugoslavica ◽

10.2298/aci0402085t ◽

2004 ◽

Vol 51 (2) ◽

pp. 85-89 ◽

Cited By ~ 4

Author(s):

R. Trzcinski ◽

M. Bry ◽

W. Krajewska ◽

M. Kulig ◽

A. Dzyiki

Keyword(s):

Inflammatory Bowel Disease ◽

Bowel Disease ◽

Intestinal Inflammation ◽

Growth Factor Receptor ◽

Experimental Colitis ◽

Altered Level ◽

Pcr Products ◽

Epidermal Growth ◽

Inflammatory Bowel ◽

Specific Symptoms

Background Ulcerative colitis (UC) and Crohn?s disease (CD) belong to inflammatory bowel disease (IBD). The etiology of IBD is still unknown. Therapy remains empiric or is used for the relief of specific symptoms. The erbB-1 oncogene coding epidermal growth factor receptor (EGFR) is typed as a prognostic marker in several benign and malignant tissues. The aim of our study was to examine the erbB-1 expression in experimental surgically performed model of IBD in rats and to find out if there is any correlation between severity of the intestinal inflammation and altered level of erbB-1 expression. After inducing an experimental colitis samples were taken from different parts of the intestine in all studied groups of rats for histopathology. ErbB-1 mRNA expression was estimated by RT-PCR. PCR products were separated on a 1,5% TBE-agarose gel and visualized with ethidium bromide. The integrated optical density (IOD) of electrophoretically separated amplification products was measured using a video densitometer and Gel-Pro 3.0 software. Nonparametrical statistical test has been used throughout in analyzing the results. Relative erbB-1 expression was determined by comparing to cyclophiline expression. Results Microscopic changes were similar to those observed in IBD. ErbB-1 expression was significantly higher in inflamed tissues of the bowel ( P=0.04 for the transverse colon and P=0.027 for the cecum). Significantly higher erbB-1 expression in inflamed tissues of the bowel suggests that EGFR overexpression may play a role in the pathogenesis of IBD. Overexpression of erbB-1 correlates with the severity of inflammation in bowel tissues.

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The Effect of α-Linolenic Acid-Rich Emulsion on Fatty Acid Metabolism and Leukotriene Generation of the Colon in a Rat Model with Inflammatory Bowel Disease

Annals of Nutrition and Metabolism ◽

10.1159/000177912 ◽

1996 ◽

Vol 40 (3) ◽

pp. 175-182 ◽

Cited By ~ 20

Author(s):

Kenichi Inui ◽

Yasuhiko Fukuta ◽

Akira Ikeda ◽

Hiromi Kameda ◽

Yukifumi Kokuba ◽

...

Keyword(s):

Inflammatory Bowel Disease ◽

Fatty Acid ◽

Linolenic Acid ◽

Fatty Acid Metabolism ◽

Rat Model ◽

Bowel Disease ◽

Acid Metabolism ◽

Alpha Linolenic Acid ◽

Inflammatory Bowel

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The in vitro anti-inflammatory effects of recombinant anti-CD25 immunotoxin on lamina propria T cells of patients with inflammatory bowel disease are not sufficient to cure experimental colitis in mice

International Journal of Colorectal Disease ◽

10.1007/s003840100336 ◽

2001 ◽

Vol 17 (2) ◽

pp. 77-84 ◽

Cited By ~ 3

Author(s):

K. Pfister ◽

B. Wittig ◽

B. Jüngling ◽

K. Ecker ◽

S. Barth ◽

...

Keyword(s):

Inflammatory Bowel Disease ◽

T Cells ◽

Lamina Propria ◽

Bowel Disease ◽

Experimental Colitis ◽

Inflammatory Bowel ◽

Anti Inflammatory

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PPARγin Inflammatory Bowel Disease

PPAR Research ◽

10.1155/2012/620839 ◽

2012 ◽

Vol 2012 ◽

pp. 1-9 ◽

Cited By ~ 39

Author(s):

Vito Annese ◽

Francesca Rogai ◽

Alessia Settesoldi ◽

Siro Bagnoli

Keyword(s):

Inflammatory Bowel Disease ◽

Bowel Disease ◽

Potential Role ◽

Intestinal Inflammation ◽

Experimental Colitis ◽

Peroxisome Proliferator ◽

Peroxisome Proliferator Activated Receptor ◽

Beneficial Effects ◽

Inflammatory Bowel

Peroxisome proliferator-activated receptor gamma (PPARγ) is member of a family of nuclear receptors that interacts with nuclear proteins acting as coactivators and corepressors. The colon is a major tissue which expresses PPARγin epithelial cells and, to a lesser degree, in macrophages and lymphocytes and plays a role in the regulation of intestinal inflammation. Indeed, both natural and synthetic PPARγligands have beneficial effects in different models of experimental colitis, with possible implication in the therapy of inflammatory bowel disease (IBD). This paper will specifically focus on potential role of PPARγin the predisposition and physiopathology of IBD and will analyze its possible role in medical therapy.

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