Induction of nitric oxide synthase and subsequent production of nitric oxide not involved in interferon-gamma-induced hyperpermeability of Caco-2 intestinal epithelial monolayers

Biosci Biotechnol Biochem. 2001 Feb;65(2):428-30. doi: 10.1271/bbb.65.428.

Abstract

Caco-2 cell monolayers exposed to 1000 U/ml interferon-gamma (IFN-gamma) for 6 days elicited inducible nitric oxide synthase (iNOS) expression and increased translayer permeability. This iNOS increase was blocked by pyrrolidinedithiocarbamate (an inhibitor of iNOS induction) but it did not suppress the hyperpermeability response. Furthermore, 2,2'-(hydroxynitrosohydrazino) bis-ethanamine (a NO donor) did not increase monolayer permeability. Therefore, IFN-gamma-induced hyperpermeability is not due to its induction of iNOS activity and resulting increases in NO levels.

MeSH terms

  • Caco-2 Cells
  • Electric Impedance
  • Enzyme Induction / drug effects
  • Epithelial Cells / drug effects
  • Epithelial Cells / metabolism
  • Humans
  • Interferon-gamma / pharmacology*
  • Intestinal Mucosa / metabolism*
  • Intestines / cytology
  • Intestines / drug effects*
  • Nitric Oxide / biosynthesis*
  • Nitric Oxide Donors / pharmacology
  • Nitric Oxide Synthase / biosynthesis*
  • Nitric Oxide Synthase Type II
  • Nitroso Compounds / pharmacology
  • Permeability
  • Recombinant Proteins
  • Tight Junctions / drug effects
  • Tight Junctions / metabolism

Substances

  • NOC 18
  • Nitric Oxide Donors
  • Nitroso Compounds
  • Recombinant Proteins
  • Nitric Oxide
  • Interferon-gamma
  • NOS2 protein, human
  • Nitric Oxide Synthase
  • Nitric Oxide Synthase Type II