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ICC density predicts bacterial overgrowth in a rat model of post-infectious IBS
Author(s): Sam-Ryong Jee, Walter Morales, Kimberly Low, Christopher Chang, Amy Zhu, Venkata Pokkunuri, Soumya Chatterjee, Edy Soffer, Jeffrey L Conklin, Mark Pimentel, GI Motility Program, Division of Gastroenterology, Cedars-Sinai Medical Center, Los Angeles, CA 90048, United States
Pages: 3680-
3686
Year: 2010
Issue:
29
Journal: World Journal of Gastroenterology
Keyword: Post-infectious irritable bowel syndrome; Bacterial overgrowth; Interstitial cells of Cajal; Campylobacter;
Abstract: AIM:To investigate the interstitial cells of Cajal(ICC) number using a new rat model.METHODS:Sprague-Dawley rats were assigned to two groups.The first group received gavage with Campylobacter jejuni(C.jejuni) 81-176.The second group was gavaged with placebo.Three months after clearance of Campylobacter from the stool,precise segments of duodenum,jejunum,and ileum were ligated in self-contained loops of bowel that were preserved in anaerobic bags.Deep muscular plexus ICC(DMP-ICC) were quantified by two blinded readers assessing the tissue in a random,coded order.The number of ICC per villus was compared among controls,Campylobacter recovered rats without small intestinal bacterial overgrowth(SIBO),and Campylobacter recovered rats with SIBO.RESULTS:Three months after recovery,27% of rats gavaged with C.jejuni had SIBO.The rats with SIBO had a lower number of DMP-ICC than controls in the jejunum and ileum.Additionally there appeared to be a density threshold of 0.12 DMP-ICC/villus that was associated with SIBO.If ileal density of DMP-ICC was < 0.12 ICC/villus,54% of rats had SIBO compared to 9% among ileal sections with > 0.12(P<0.05).If the density of ICC was < 0.12 DMP-ICC/villus in more than one location of the bowel,88% of these had SIBO compared to 6% in those who did not(P<0.001).CONCLUSION:In this post-infectious rat model,the development of SIBO appears to be associated with a reduction in DMP-ICC.Further study of this rat model might help understand the pathophysiology of postinfectious irritable bowel syndrome.
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