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Investigating Intestinal Inflammation in DSS-induced Model of IBD
Published on: February 1, 2012
Altered response to hydrogen sulphide during experimental colitis in rats
J Steidle1, L Würner1, M Diener1
1Institute for Veterinary Physiology and Biochemistry, Justus-Liebig-University Giessen, Giessen, Germany.
Journal of Animal Physiology and Animal Nutrition
|September 12, 2012
Summary
Hydrogen sulphide (H2S) plays a complex role in colitis. Inflammation reduced the gut
Area of Science:
- Gastroenterology
- Physiology
- Microbiology
Background:
- Hydrogen sulphide (H2S) is an endogenous gasotransmitter produced in the gut.
- H2S influences intestinal anion secretion and has debated pro- and anti-inflammatory roles.
Purpose of the Study:
- To investigate the role of H2S in experimental colitis.
- To compare the effects of blocking H2S-producing enzymes versus a sulfur-reduced diet.
Main Methods:
- Chronic colitis induced via rectal trinitrobenzenesulfonic acid (TNBS) administration.
- Inflammation assessed macroscopically and histologically.
- Ussing chamber experiments to measure colonic epithelial permeability and ion transport.
- Evaluated responses to exogenous H2S donor (NaHS) and other secretagogues.
Main Results:
- TNBS-induced colitis increased colonic tissue conductance (permeability).
- The secretory response to exogenous H2S was significantly decreased in colitis models.
- A sulfur-reduced diet prevented this H2S response downregulation.
- Responses to calcium or cAMP-dependent secretagogues remained unaltered.
Conclusions:
- Colonic inflammation leads to desensitization to exogenous H2S.
- This desensitization may involve upregulated endogenous H2S production during inflammation.
- Dietary modification (sulfur reduction) can mitigate inflammation-induced changes in H2S responsiveness.
