Host anti-CdtB antibodies cross-react with vinculin in ICC and myenteric ganglia, required for normal gut motility. Circulating antibody levels and loss of vinculin expression correlate with number of C. jejuni exposures and SIBO, suggesting that effects on vinculin are important in the effects of C. jejuni infection on the host gut.

Studies suggest that subjects with IBS have altered gut flora. Among these findings, methane production is more commonly associated with constipation-predominant symptoms. In this study, we prospectively evaluated the role of methane as a diagnostic test. Consecutive Rome I positive IBS patients referred for a lactulose breath test were eligible to participate. After exclusion criteria, subjects completed a symptom questionnaire grading bloating, diarrhea, and constipation on a VAS scale (0-100 mm). Once completed, a physician interviewed the subjects and rated the subject accordingly, and also determined whether the patient had C-IBS, D-IBS, or neither. Subjects and physicians were blinded to the results of the breath test. The presence of methane in the breath test was compared to the results of the scoring by subjects and physicians. A total of 56 Rome I positive IBS subjects were enrolled. During breath testing, 28 subjects produced methane. Good agreement between physician's evaluation and the patient's was seen (diarrhea = 0.69; constipation = 0.69; bloating = 0.62). The severity of constipation was noted to be greater in the methane group (49.3 +/- 28.7) than in the non-methane group (25.3 +/- 31.47) (P < 0.01). In contrast, diarrhea was less severe in the methane group (12.3 +/- 21.0) than the non-methane group (36.7 +/- 32.4) (P < 0.01). Out of the 56 patients, 23 C-IBS subjects were identified by the physician. When methane was used to predict the assignment of C-IBS compared to non-C-IBS, it had a sensitivity of 91.7% and a specificity of 81.3% (OR = 47.7, CI = 9.4-232, P < 0.00001). In conclusion, methane is a potential diagnostic test for the identification of C-IBS and may guide treatment.

Background/AimsCampylobacter jejuni infection is a leading cause of acute gastroenteritis, which is a trigger for post-infectious irritable bowel syndrome (PI-IBS). Cytolethal distending toxin (CDT) is expressed by enteric pathogens that cause PI-IBS. We used a rat model of PI-IBS to investigate the role of CDT in long-term altered stool form and bowel phenotypes.MethodsAdult Sprague-Dawley rats were gavaged with wildtype C. jejuni (C+), a C. jejuni cdtB knockout (CDT-) or saline vehicle (controls). Four months after gavage, stool from 3 consecutive days was assessed for stool form and percent wet weight. Rectal tissue was analyzed for intraepithelial lymphocytes, and small intestinal tissue was stained with anti-c-kit for deep muscular plexus interstitial cells of Cajal (DMP-ICC).ResultsAll 3 groups showed similar colonization and clearance parameters. Average 3-day stool dry weights were similar in all 3 groups, but day-to-day variability in stool form and stool dry weight were significantly different in the C+ group vs both controls (P < 0.01) and the CDT- roup (P < 0.01), but were not different in the CDT- vs controls. Similarly, rectal lymphocytes were significantly higher after C. jejuni (C+) infection vs both controls (P < 0.01) and CDT-exposed rats (P < 0.05). The counts in the latter 2 groups were not significantly different. Finally, c-kit staining revealed that DMP-ICC were reduced only in rats exposed to wildtype C. jejuni.ConclusionsIn this rat model of PI-IBS, CDT appears to play a role in the development of chronic altered bowel patterns, mild chronic rectal inflammation and reduction in DMP-ICC.

Retreatment with rifaximin for subjects with nonconstipated IBS in a real-world clinical practice was successful up to five times without decrease in duration or effect.

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 post-infectious irritable bowel syndrome.