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Endogenous hydrogen sulfide contributes to visceral hypersensitivity in irritable bowel syndrome

 

 

 

 

Mol Pain. 2009 Aug 6;5(1):44. [Epub ahead of print]

 

The endogenous hydrogen sulfide producing enzyme cystathionine-beta synthase contributes to visceral hypersensitivity in a rat model of irritable bowel syndrome.

 

Xu GY, Winston JH, Shenoy M, Zhou S, Chen JD, Pasricha PJ.

 

 

BACKGROUND: The pathogenesis of visceral hypersensitivity, a characteristic pathophysiological feature of irritable bowel syndrome (IBS), remains elusive. Recent studies suggest a role for hydrogen sulfide (H2S) in pain signaling but this has not been well studied in visceral models of hyperalgesia. We therefore determined the role for the endogenous H2S producing enzyme cystathionine-beta-synthetase (CBS) in a validated rat model of IBS-like chronic visceral hyperalgesia (CVH). CVH was induced by colonic injection of 0.5% acetic acid (AA) in 10-day-old rats and experiments were performed at 8-10 weeks of age. Dorsal root ganglion (DRG) neurons innervating the colon were labeled by injection of DiI (1,1'-dioleyl-3,3,3',3-tetramethylindocarbocyanine methanesulfonate) into the colon wall.

 

RESULTS: In rat DRG, CBS-immunoreactivity was observed in approximately 85% of predominantly small- and medium-sized neurons. Colon specific DRG neurons revealed by retrograde labeling DiI were all CBS-positive. CBS-positive colon neurons co-expressed TRPV1 or P2X3 receptors. Western blotting analysis showed that CBS expression was significantly increased in colon DRGs 8 weeks after neonatal AA-treatment. Furthermore, the CBS inhibitor hydroxylamine markedly attenuated the abdominal withdrawal reflex scores in response to colorectal distention in rats with CVH. By contrast, the H2S donor NaHS significantly enhanced the frequency of action potentials of colon specific DRG neurons evoked by 2 times rheobase electrical stimulation.

 

CONCLUSION: Our results suggest that upregulation of CBS expression in colonic DRG neurons and H2S signaling may play an important role in developing CVH, thus identifying a specific neurobiological target for the treatment of CVH in functional bowel syndromes.

 

PMID: 19660142 [PubMed - as supplied by publisher]

 

 

 

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  • The findings reported here that increased H2S may be a cause of the abdominal pain associated with IBS is very interesting, expecially in light of recent developments in the chronic fatigue syndrome (ME/CFS) community. In the study reported here the H2S is produced by one of the body's own enzymes (cystathionine-beta-synthetase (CBS)) but ME/CFS researchers have noted that H2S can also be produced by various bacteria in the gut. Small intestinal bacterial overgrowth (SIBO) has been found in IBS patients so could gut bacteria also be contributing to the production of H2S in IBS patients? Let's hope further research answers this intriguing question.

    See this coverage of H2S and ME/CFS by Dr. Jacob Teitelbaum - [URL=http://www.ei-resource.org/expert-columns/dr.-jacob-teitelbaums-column/smelly-gas-a-clue-to-cfs-testing-and-treatment/]Smelly Gas a Clue to CFS Testing and Treatment[/url].

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