Local regulation of immune and inflammatory responses within the alveolar space is a critical aspect of normal pulmonary host defense. The type I and type II epithelial cells that line the alveolar space are in intimate contact with lymphocytes and macrophages within the alveolar space and are ideally situated to provide regulatory signals to these effector cells. The present studies were undertaken to investigate the expression by rat alveolar epithelial cells in vitro and in vivo of intercellular adhesion molecule-1 (ICAM-1), an adhesion molecule that is involved in migration and activation of T cells and macrophages. An antibody specifically blocking rat ICAM-1 (mAb 1A29) inhibited the adherence of activated T lymphoblasts to monolayers of type II alveolar epithelial cells. The expression of ICAM-1 protein by alveolar epithelial cells in vitro was confirmed both by immunofluorescence microscopy and by Western blot analysis. However, in each instance, ICAM-1 was not detected in type II cells the day of isolation, but appeared at low levels after 1 day and in abundance throughout the monolayer after 2 days, with sustained expression thereafter. This suggested that ICAM-1 expression might be a type I cell feature, which was induced as isolated type II cells underwent transformation towards the type I cell-like phenotype in vitro. Using immunofluorescence microscopy on frozen sections of normal lung, ICAM-1 was found in a linear distribution along the alveolar space, consistent with expression on type I cells.(ABSTRACT TRUNCATED AT 250 WORDS)