Hyperthermia prevents functional, histological and biochemical abnormalities induced during ileitis

J. M. Goldhill, A. Stojadinovic, J. Kiang, R. Smallridge, T. Shea-Donohue

Research output: Contribution to journalArticle

12 Scopus citations

Abstract

Inflammatory bowel disease is associated with altered intestinal motility and epithelial damage. Hyperthermia induces heat shock protein expression, components of a basic cellular defence mechanism, and consequently prevents ischaemic damage. Here we investigate whether hyperthermia may prevent altered smooth muscle function as well as underlying inflammation in a model of inflammatory bowel disease. Ileal heat shock protein expression was induced in rats by hyperthermic shock (41.5°C; 5 min). Two hours after heating or sham treatment, ileitis was evoked by TNBS. Ileal samples were taken 4 h later to determine the contractile response of circular muscle strips, and to measure heat shock protein expression, LTB4 generation and damage/inflammation. Ileitis was associated with an increase in the contractile response of circular muscle to substance P but not neurokinin A or nerve stimulation. Hyperthermia induced heat shock protein expression and also prevented this functional change as well as TNBS-induced LTB4 production, subsequent infiltration of neutrophils and epithelial damage. Thus, intestinal inflammation is associated with alterations in tachykinergic control of smooth muscle as well as inflammatory changes. Hyperthermia prevents these changes and induces heat shock protein expression. Pharmacological induction of these proteins may offer a novel clinical strategy in treating both of these aspects of disease.

Original languageEnglish (US)
Pages (from-to)69-76
Number of pages8
JournalNeurogastroenterology and Motility
Volume11
Issue number1
DOIs
StatePublished - Feb 24 1999

Keywords

  • Anti-inflammatory
  • Heat-shock protein
  • Ileitis
  • Inflammatory bowel disease
  • Substance P
  • Tachykinin

ASJC Scopus subject areas

  • Physiology
  • Endocrine and Autonomic Systems
  • Gastroenterology

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