title: Host immune response determines visceral hyperalgesia in a rat model of post-inflammatory irritable bowel syndrome.
abstract: BACKGROUND
  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 (99m)Tc-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 (99m)Tc-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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Bone Marrow Transplantation, University Hospital Essen, University Duisburg-Essen, West German Cancer Center, Hufelandstr. 55, 45122, Essen, Germany, birgit.adam@uk-essen.de.
authors.forename: Birgit
authors.initials: B
authors.lastname: Adam
authors.forename: Chris
authors.initials: C
authors.lastname: Tsopelas
authors.forename: Tobias
authors.initials: T
authors.lastname: Liebregts
authors.forename: F Dylan
authors.initials: FD
authors.lastname: Bartholomeusz
authors.forename: Gerald
authors.initials: G
authors.lastname: Holtmann
mesh_terms: D000818:Animals; D003092:Colitis / Q000139:chemically induced / Q000276:immunology*; D003106:Colon / Q000473:pathology*; D004195:Disease Models, Animal; D006930:Hyperalgesia / Q000276:immunology* / Q000473:pathology; D007376:Interleukin-2 / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D043183:Irritable Bowel Syndrome / Q000276:immunology* / Q000473:pathology; D008297:Male; D051381:Rats; D011916:Rats, Inbred F344; D011917:Rats, Inbred Lew; D014302:Trinitrobenzenesulfonic Acid
chemical_list: D007376:Interleukin-2; D015850:Interleukin-6; D014302:Trinitrobenzenesulfonic Acid