The distribution of intercellular adhesion molecule-l (ICAM-l) on alveolar epithelial cells and the effects of exposure to 100% O2 on ICAM-l 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-l antibody. In the normal lung, abundant ICAM-l expression was found on the alveolar surface of type I epithelial cells. Furthermore, ICAM-l is highly concentrated on the surfaces near cell junctions. ICAM-l 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-l on the central surface of type I epithelial cells was not changed significantly. However, the gradient of ICAM-l on the surfaces near cell junctions was nearly abolished. ICAM-l labeling on the capillary surface of endothelial cells remained low. ICAM-l was also markedly induced on the alveolar surface of type II epithelial cells after hyperoxic exposure. These results show that ICAM-l 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-l on alveolar type I epithelial cells and induces expression oflCAM-l 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.

Intercellular adhesion molecule-l (ICAM-l) is a single-chain cell surface glycoprotein with molecular masses of 76 to 114 kD (1-4). It is a member of the immunoglobulin superfamily consisting of five immunoglobulin-like domains in its extracellular portion (5, 6). ICAM-l is expressed at low level on a variety of cells, including vascular endothelium, and is involved in intercellular adhesion as well as leukocyte adhesion and migration (1-4).