The effect of cytokine stimulation on IL-1 receptor mRNA expression by intestinal epithelial cells

Cell Immunol. 1996 Mar 15;168(2):276-80. doi: 10.1006/cimm.1996.0076.

Abstract

Interleukin-1 (IL-1) can induce intestinal epithelial cells (IEC) to produce several cytokines and acute phase proteins, suggesting that IEC may be important in a cytokine network at the intestinal mucosa to amplify the effects of IL-1 during an inflammatory response. However, little is known about the type of IL-1 receptor expressed by IEC and the effect of cytokines on the expression of these receptors. In this study, the expression by IEC of IL-1 receptor Type I (IL-1RI) and type II (IL-1RII) mRNA was examined by reverse transcriptase polymerase chain reaction. Both isolated rat IEC and the rat IEC-6 intestinal epithelial cell line were found to express mRNA for IL-1RI but not IL-1RII. Stimulation of the IEC-6 cells with IL-1beta or TNF-alpha down-regulated the expression of mRNA for IL-1RI at 24 hr, yet transforming growth factor-beta1 was found to have no effect. These results suggest a possible mechanism to limit the effect of IL-1 on IEC function during the mucosal inflammatory response by down-regulating the expression of the Type I IL-1 receptor.

Publication types

  • Comparative Study
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Cell Line
  • Down-Regulation / drug effects*
  • Epithelium / metabolism
  • Humans
  • Interleukin-1 / pharmacology*
  • Intestinal Mucosa / metabolism*
  • Mice
  • RNA, Messenger / analysis
  • RNA, Messenger / biosynthesis
  • Rats
  • Rats, Inbred F344
  • Receptors, Interleukin-1 / biosynthesis*
  • Receptors, Interleukin-1 / classification
  • Receptors, Interleukin-1 / genetics
  • Recombinant Proteins / pharmacology
  • Species Specificity
  • Spleen / cytology
  • Swine
  • Transforming Growth Factor beta / pharmacology*
  • Tumor Necrosis Factor-alpha / pharmacology*

Substances

  • Interleukin-1
  • RNA, Messenger
  • Receptors, Interleukin-1
  • Recombinant Proteins
  • Transforming Growth Factor beta
  • Tumor Necrosis Factor-alpha