PHENOTYPING AND CYTOKINE REGULATION OF THE BEAS-2B HUMAN BRONCHIAL EPITHELIAL-CELL - DEMONSTRATION OF INDUCIBLE EXPRESSION OF THE ADHESION MOLECULES VCAM-1 AND ICAM-1

Airway epithelium may actively participate in inflammatory responses, such as occur in asthma. The presence and regulation of surface molecu les on the airway epithelium, however, is incompletely understood. We have determined the phenotype of the human bronchial epithelial cell l ine BEAS-2B by flow cytometry. We confirmed previous observations that human bronchial epithelial cells constitutively express CD29, CD44, C D49a, CD49b, CD49c, CD49d, CD49e, CD49f, CD51, CD54 (ICAM-1), CD61, an d HLA class 1. BEAS-2B cells were also found to constitutively express CD9, CD13, CD15, CD15s, CD23, CD33, CD36, CD40, CD41b, CD42b, CD48, C D50, CD71, and CD102 (ICAM-2). Culture of BEAS-2B cells with tumor nec rosis factor (TNF)-alpha or interleukin (IL)-1 beta (1 ng/ml) was foun d to enhance intercellular adhesion molecule-1 (ICAM-1) expression (se veralfold) and induce de novo CD106 [vascular cell adhesion molecule-1 (VCAM-1)] expression. TNF-alpha or IL-1 beta did not change the expre ssion of CD9, CD13, CD16, CD23, CD29, CD31, CD32, CD35, CD45, CD61, or CD64 in BEAS-2B cells. IL-4 (1 ng/ml) also induced expression of VCAM -1 (1.5-fold) but not ICAM-1 expression while interferon-gamma (1 ng/m l) enhanced only ICAM-1 expression (2-fold). Maximal VCAM-1 expression was obtained with the combination of TNF-alpha and IL-4 (8-fold). Usi ng Northern blot hybridization analysis, ICAM-1 and VCAM-1 mRNA was de tected in BEAS-2B cells stimulated with cytokines. VCAM-1 on stimulate d BEAS-2B was functionally active as determined by adhesion of purifie d eosinophils and blockade with specific antibodies. Primary isolates of bronchial epithelial cells produced detectable levels of VCAM-1 pro tein and mRNA as detected by enzyme-linked immunosorbent assay and rev erse transcription-polymerase chain reaction, respectively. These resu lts suggest that cytokine activation induces expression of ICAM-1 and VCAM-1 on airway epithelium, an event which may influence leukocyte in filtration and activation.