IL-1 stimulates intestinal myofibroblast COX gene expression and augments activation of Cl- secretion in T84 cells

Thomas A. Hinterleitner, Jamal I. Saada, Helen M. Berschneider, Don W. Powell, John D. Valentich

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Abstract

Because interleukin-1 (IL-1) is an important mediator in the inflamed intestine, its effects on enterocyte-subepithelial myofibroblast (SEMF) interaction were investigated in vitro. Acutely juxtaposing T84 cells with 18Co or P2JF SEMF preincubated with IL-1α significantly enhanced T84 short- circuit current (I(sc)) responsiveness to secretagogues in comparison to SEMF not activated by IL-1α. The sensitivity of T84 cell I(sc) to Ca2+- dependent, but not adenosine 3',5'-cyclic monophosphate-dependent, secretagogues was augmented by IL-1α-treated SEMF. These effects of IL-1α are directly correlated with SEMF prostaglandin E2 (PGE2) production. Both IL-1α augmentation of Cl- secretagogue responsiveness and PGE2 formation were inhibited by IL-1 receptor antagonist. Within 5 h, IL-1α stimulated a 10-fold increase in cyclooxygenase (COX)-2 steady-state mRNA levels in 18Co cells. In contrast, COX-1 message levels increased more slowly to two- to threefold above control levels after 24 h incubation. These results demonstrate that the proinflammatory cytokine IL-1α accentuates intestinal SEMF augmentation of enterocyte responsiveness to Ca2+-dependent Cl- secretagogues. PGE2 is an important mediator of SEMF-enterocyte interaction. The effects of IL-1α on SEMF PGE2 productions are, at least in part, due to stimulation of COX gene expression.

Original languageEnglish (US)
Pages (from-to)C1262-C1268
JournalAmerican Journal of Physiology - Cell Physiology
Volume271
Issue number4 40-4
StatePublished - Oct 1 1996

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Keywords

  • cyclooxygenase
  • interleukin-1
  • intestines
  • prostaglandins

ASJC Scopus subject areas

  • Physiology
  • Cell Biology

Cite this

Hinterleitner, T. A., Saada, J. I., Berschneider, H. M., Powell, D. W., & Valentich, J. D. (1996). IL-1 stimulates intestinal myofibroblast COX gene expression and augments activation of Cl- secretion in T84 cells. American Journal of Physiology - Cell Physiology, 271(4 40-4), C1262-C1268.