Host immune response determines visceral hyperalgesia in a rat model of post-inflammatory irritable bowel syndrome

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dc.contributor.authorAdam, B.
dc.contributor.authorTsopelas, C.
dc.contributor.authorLiebregts, T.
dc.contributor.authorBartholomeusz, F.
dc.contributor.authorHoltmann, G.
dc.date.issued2013
dc.description.abstractBACKGROUND Irritable bowel syndrome (IBS) is associated with visceral hyperalgesia and frequently occurs after a transient gastrointestinal infection. Only a proportion of patients with acute gastroenteritis develop post-infectious IBS suggesting differences in host response to inflammatory stimuli. We aimed to investigate this concept by characterizing visceral sensitivity in two rat strains, following a chemically induced colitis. METHODS Colorectal instillation of trinitrobenzenesulfonic acid (TNBS) in aqueous ethanol was used to induce a transient colitis in Lewis and F344 rats. The colitis was characterized semiquantitatively by histology, as well as by quantitative methods using 99mTc-leukocytes (radioactive organ assay) and plasma IL-2 and IL-6 levels. Visceromotor response to colorectal distensions was assessed after 2 h and, 5, 14, and 28 days. RESULTS The colitis peaked on day 5 and dissipated to no visible mucosal damage on day 14. Cytokines were significantly increased in TNBS-treated rats at 2 h and on day 5. On day 14 cytokines were still significantly enhanced in Lewis but not Fisher rats. Both strains had a highly inflamed to non-inflamed tissue ratio at 3 h after TNBS instillation with increased uptake in Lewis compared to F344 rats. No 99mTc-tin-colloid-leukocytes were detected in colon samples on day 28. Visceromotor response was significantly elevated in both strains during the acute colitis (day 5), whereas only Lewis rats developed a post-inflammatory (day 28) visceral hyperalgesia. CONCLUSION Genetically determined host factors account for prolonged immune activation in response to a standardized inflammatory stimulus and are linked to susceptibility for a post-inflammatory visceral hyperalgesia.
dc.description.statementofresponsibilityBirgit Adam, Chris Tsopelas, Tobias Liebregts, F. Dylan Bartholomeusz, Gerald Holtmann
dc.identifier.citationJournal of Gastroenterology, 2013; 48(10):1119-1127
dc.identifier.doi10.1007/s00535-012-0729-2
dc.identifier.issn0944-1174
dc.identifier.issn1435-5922
dc.identifier.urihttp://hdl.handle.net/2440/81504
dc.language.isoen
dc.publisherSpringer-Verlag
dc.rights© Springer Japan 2012
dc.source.urihttps://doi.org/10.1007/s00535-012-0729-2
dc.subjectInflammation
dc.subjectVisceral hyperalgesia
dc.subjectCytokines
dc.subjectIrritable bowel syndrome
dc.subjectGenetic factors
dc.titleHost immune response determines visceral hyperalgesia in a rat model of post-inflammatory irritable bowel syndrome
dc.typeJournal article
pubs.publication-statusPublished

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