Intercellular adhesion molecule-1 expression on the alveolar epithelium and its modification by hyperoxia.

Abstract

The distribution of intercellular adhesion molecule-1 (ICAM-1) on alveolar epithelial cells and the effects of exposure to 100% O2 on ICAM-1 expression in mouse lungs were studied by EM immunocytochemistry and immunoblot analysis. Cryoultrathin sections from mouse lungs exposed to air or 100% O2 for 84 h were labeled with a monoclonal rat anti-mouse ICAM-1 antibody. In the normal lung, abundant ICAM-1 expression was found on the alveolar surface of type I epithelial cells. Furthermore, ICAM-1 is highly concentrated on the surfaces near cell junctions. ICAM-1 was also found on the capillary surface of endothelial cells and alveolar surface of type II cells at densities considerably lower than that found on type I epithelial cells. After exposure to O2, the labeling density of ICAM-1 on the central surface of type I epithelial cells was not changed significantly. However, the gradient of ICAM-1 on the surfaces near cell junctions was nearly abolished. ICAM-1 labeling on the capillary surface of endothelial cells remained low. ICAM-1 was also markedly induced on the alveolar surface of type II epithelial cells after hyperoxic exposure. These results show that ICAM-1 is expressed primarily on type I epithelial cell surfaces near cell junctions. Exposure to hyperoxia causes a dramatic change in the distribution pattern of ICAM-1 on alveolar type I epithelial cells and induces expression of ICAM-1 on alveolar type II epithelial cells. These hyperoxia-induced changes may influence the associated neutrophil invasion/retention in the alveolar air spaces or alveolar walls.