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Interleukins 1 and 3 stimulate anion secretion in chicken intestine

E B Chang1, M W Musch, L Mayer

  • 1Department of Medicine, University of Chicago, Illinois.

Gastroenterology
|June 1, 1990
PubMed

Insights

Cytokines like interleukin 1 and 3 enhance intestinal anion secretion via prostaglandin production. This process, involving subepithelial cells, may contribute to inflammation-driven intestinal hypersecretion.

Area of Science:

  • Gastroenterology
  • Immunology
  • Cell Biology

Background:

  • Interleukins (ILs) are key immune signaling molecules.
  • Cytokines are known to influence various physiological processes, including intestinal function.
  • Understanding cytokine-mediated signaling in the intestine is crucial for inflammatory bowel disease research.

Purpose of the Study:

  • To investigate the role of Interleukin 1 (IL-1) and Interleukin 3 (IL-3) in regulating chicken small intestine secretion.
  • To elucidate the signaling pathways involved in cytokine-induced intestinal secretion, focusing on prostaglandins and cyclic adenosine monophosphate (cAMP).
  • To identify the cellular sources of prostaglandin production stimulated by cytokines in the intestinal mucosa.

Main Methods:

  • Short-circuit current (SCC) measurements on chicken small intestine serosal side.
  • Ion replacement studies using gluconate and HEPES to assess anion secretion.
  • Pharmacological inhibition using piroxicam, an inhibitor of cyclooxygenase.
  • Measurement of prostaglandin E2 (PGE2) release from mucosal tissues.
  • Quantification of 3',5'-cyclic adenosine monophosphate (cAMP) levels in intestinal tissue.

Main Results:

  • IL-1 and IL-3 significantly increased SCC, indicating stimulated electrogenic anion secretion.
  • The increase in SCC was abolished by replacing bathing medium ions and by piroxicam preincubation, implicating prostaglandins.
  • Both IL-1 and IL-3 stimulated PGE2 release and elevated cAMP levels in intact mucosal strips.
  • PGE2 release was primarily observed from subepithelial fractions, not epithelial cells, upon IL-1 stimulation.

Conclusions:

  • Cytokine-induced intestinal secretion is mediated by prostaglandins, likely produced by subepithelial cells (lamina propria and submucosa).
  • Arachidonic acid metabolites play a critical role in the secretory actions of IL-1 and IL-3 in the chicken small intestine.
  • These findings suggest a mechanism by which cytokines can enhance intestinal secretion during inflammatory processes.

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