Bh. Kang et al., INTERCELLULAR-ADHESION MOLECULE-1 EXPRESSION ON THE ALVEOLAR EPITHELIUM AND ITS MODIFICATION BY HYPEROXIA, American journal of respiratory cell and molecular biology, 9(4), 1993, pp. 350-355
The distribution of intercellular adhesion molecule-1 (ICAM-1) on alve
olar 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 t
o air or 100% O2 for 84 h were labeled with a monoclonal rat anti-mous
e 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. IC
AM-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 labe
ling density of ICAM-1 on the central surface of type I epithelial cel
ls was not changed significantly. However, the gradient of ICAM-1 on t
he 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 c
ells after hyperoxic exposure. These results show that ICAM-1 is expre
ssed primarily on type I epithelial cell surfaces near cell junctions.
Exposure to hyperoxia causes a dramatic change in the distribution pa
ttern of ICAM-1 on alveolar type I epithelial cells and induces expres
sion of ICAM-1 on alveolar type II epithelial cells. These hyperoxia-i
nduced changes may influence the associated neutrophil invasion/retent
ion in the alveolar air spaces or alveolar walls.