IL-1beta and TNFalpha regulate sodium absorption in rat distal colon

Biochem Biophys Res Commun. 2004 Apr 30;317(2):500-7. doi: 10.1016/j.bbrc.2004.03.072.

Abstract

The epithelial Na+ channel (ENaC) provides the main absorptive pathway of the distal large intestine. This study aimed to characterize regulatory influences of cytokines in rat late distal colon. After 6 h incubation with either IL1beta, TNFalpha, IFNgamma, or combinations of TNFalpha and IFNgamma, ENaC was measured as electrogenic Na+ transport after 8 h induction by 3 nM aldosterone (JNa) in totally stripped specimens in the Ussing chamber. Subsequently, alpha-, beta-, and gamma-ENaC subunit mRNAs were analyzed by Northern blotting. The gamma-ENaC promoter was cloned and characterized by reporter gene assays. IL-1beta and TNFalpha, but not interferon-gamma, decreased JNa. In parallel, beta- and gamma-ENaC transcription was inhibited, whereas alpha-ENaC was unaffected. gamma-ENaC promoter activity was inhibited by IL-1beta and TNFalpha but not by IFNgamma. We conclude that the pro-inflammatory cytokines IL-1beta and TNFalpha inhibit electrogenic sodium absorption in rat distal colon by mRNA expression regulation of the beta- and gamma-ENaC subunits.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aldosterone / pharmacology
  • Animals
  • Cell Line
  • Cells, Cultured
  • Epithelial Sodium Channels
  • Humans
  • Interferon-gamma / metabolism*
  • Interleukin-1 / metabolism*
  • Intestinal Mucosa / drug effects
  • Intestinal Mucosa / metabolism*
  • Intestines / drug effects
  • Male
  • Rats
  • Sodium / pharmacokinetics*
  • Sodium Channels / drug effects
  • Sodium Channels / physiology*
  • Tumor Necrosis Factor-alpha / metabolism*

Substances

  • Epithelial Sodium Channels
  • Interleukin-1
  • Sodium Channels
  • Tumor Necrosis Factor-alpha
  • Aldosterone
  • Interferon-gamma
  • Sodium