Selective inflammatory cell infiltration of the airway is an important component of many respiratory diseases. An increase in neutrophils is seen in acute bronchitis, chronic obstructive pulmonary disease, adult respiratory distress syndrome, and cystic fibrosis (1,2) whereas, an increase in T-lymphocytes is seen in sarcoidosis, hypersensitivity pneumonitis, and radiation pneumonitis (3,4,5); some diseases, such as asthma, show an influx of both of these cell types (6,7). In order to reach the airway, leukocytes in the blood must adhere to and migrate through the vascular endothelium, and then undergo a similar sequence of events to cross the bronchial epithelium. While the mechanisms involve in the interactions with the endothelium have been well studies, little is known about the process governing the movement of specific leukocyte subsets through the epithelial barrier. We hypothesize that, in a comparable manner to leukocyte-endothelial interactions, adhesion of neutrophils and T-lymphocytes to airway epithelium is mediated by specific families of adhesion molecules and by the activation status of each cell type, and the subsequent transepithelial migration occurs in response to specific chemotactic factors. These cell-specific recruitment mechanisms determine whether an influx of neutrophils or T- lymphocytes is seen in a certain disease state. We will use neutrophils and T-lymphocytes isolated from normal human subjects and a human bronchial epithelial cell line (BEAS-2B) to study these processes.
