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Dig Dis Sci. 2008 Apr;53(4):982-9. Epub 2007 Oct 13.

A new rat model links two contemporary theories in irritable bowel syndrome.

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GI Motilty Program, Cedars-Sinai Medical Center, Burns and Allen Research Institute, 8730 Alden Drive, Suite 225E, Los Angeles, CA 90048, USA.



Two proposed hypotheses for irritable bowel syndrome (IBS) are acute gastroenteritis and bacterial overgrowth. We studied whether acute infection with Campylobacter could precipitate bacterial overgrowth in a rat model in order to link the two hypotheses.


Sprague-Dawley outbred rats were randomly administered a vehicle or Campylobacter jejuni strain 81-176 by oral gavage. Three months after clearance of the infectious agent, rats had a stool consistency evaluation. After euthanasia, lumenal bacteria counts were measured via quantitative real-time PCR from self-contained segments of the duodenum, jejunum, ileum, cecum and left colon. Adjacent sections of bowel were fixed in formalin for evaluation of intraepithelial lymphocyte counts.


Three months after clearance of Campylobacter infection, 57% of Campylobacter infected rats had some alteration in stool consistency compared to 7.4% in mock-infected controls (P < 0.001). Among the rats that received Campylobacter, 27% had evidence of bacterial overgrowth by PCR. These rats also had the highest prevalence of altered stool form and had lower body weight. Consistent with post-infectious IBS in humans, bacterial overgrowth rats demonstrated a significant increase in rectal and left colon intraepithelial lymphocytes.


Acute infection with C. jejuni 81-176 precipitates alterations in stool consistency, bacterial overgrowth and rectal lymphocytosis consistent with findings in IBS patients.

[Indexed for MEDLINE]

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