Previous inflammation alters the response of the rat colon to stress

Gastroenterology. 1996 Dec;111(6):1509-15. doi: 10.1016/s0016-5085(96)70012-4.


Background & aims: Patients with inflammatory bowel disease have symptoms of irritable bowel syndrome (IBS) with a higher than expected prevalence. Stress is an important factor in the pathogenesis of IBS. Thus, previous inflammation may predispose to IBS by rendering the bowel more susceptible to the impact of stress. The aim of this study was to examine the effect of previous colitis on stress-induced responses in rats.

Methods: Acute colitis was induced in rats by intrarectal administration of trinitrobenzene sulfonic acid (TNBS), and the rats were allowed to recover for 6 weeks before application of mild restraint stress for 3 consecutive days. In vitro measurements included myeloperoxidase activity, plasma corticosterone levels, interleukin 1 beta messenger RNA expression, and [3H]noradrenaline release from the myenteric plexus.

Results: Six weeks after administration of TNBS, stress caused a significant increase in myeloperoxidase activity in TNBS-treated rats but not in stressed controls; plasma corticosterone responses were similar. Stress also caused an exaggerated and significant suppression of [3H]noradrenaline release in TNBS-treated stressed rats compared with stressed controls. This was accompanied by a significant decrease in interleukin 1 beta messenger RNA expression in the colon.

Conclusions: Previous colitis rendered the colon more susceptible to effects of stress on enteric nerve function and also increased some parameters of inflammation in response to stress.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Colitis / chemically induced
  • Colitis / metabolism
  • Colitis / physiopathology*
  • Colon / metabolism
  • Colon / physiopathology*
  • Corticosterone / blood
  • Interleukin-1 / analysis
  • Male
  • Norepinephrine / analysis
  • Peroxidase / analysis
  • Rats
  • Rats, Inbred WKY
  • Rats, Sprague-Dawley
  • Stress, Physiological*
  • Trinitrobenzenesulfonic Acid / toxicity


  • Interleukin-1
  • Trinitrobenzenesulfonic Acid
  • Peroxidase
  • Corticosterone
  • Norepinephrine