Abstract
Caco-2 cell monolayers exposed to 1000 U/ml interferon-γ (IFN-γ) 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-γ-induced hyperpermeability is not due to its induction of iNOS activity and resulting increases in NO levels.
