IL-4 directly modulates function of a model human intestinal epithelium.

摘要: Intestinal epithelia are in intimate contact with subepithelial and intraepithelial lymphocytes. When stimulated, mucosal lymphocytes generate inflammatory cytokines such as IL-4 IFN-gamma. We have shown that IFN-gamma directly regulates epithelial function. It is unknown whether might influence function and, if so, influences similar to or differ from those exerted by In this study, we examine the effect of human on barrier function, ion transport, immune accessory ligand expression T84 cells, a crypt-like cell line. Basolateral exposure monolayers attenuated greater than 65% dose (50% effective = 1 U/ml)- time (t1/2 24 h)-dependent fashion, was inhibitable neutralizing anti-IL-4 anti-IL-4R Ab. Stimulated Cl- secretion, measured short circuit current, diminished much 70% IL-4. Epithelial preexposure brought about twofold increase beta 2 integrin-dependent neutrophil adhesion epithelial, but retarded migration into across monolayers. ELISAs revealed had no surface MHC class I, II, ICAM-1. These results indicate IL-4, like IFN-gamma, may serve regulate intestinal resulting phenotypes be cytokine specific. speculate these data activation basolateral receptor for potentially provides new strategy damping cellular component active inflammation intestine.