Respiratory syncytial virus infection of human lung endothelial cells enhances selectively intercellular adhesion molecule-1 expression.

摘要: Respiratory syncytial virus (RSV) is worldwide the most frequent cause of bronchiolitis and pneumonia in infants requiring hospitalization. In present study, we supply evidence that human lung microvascular endothelial cells, pulmonary aorta HUVEC are target cells for productive RSV infection. All three RSV-infected cell types showed an enhanced surface expression ICAM-1 (CD54), which increased a time- RSV-dose-dependent manner. By using noninfectious particles verified replication prerequisite increase expression. The up-regulated pattern correlated with cellular mRNA amount. contrast to ICAM-1, de novo VCAM-1 (CD106) was only observed on HUVEC. Neither P-selectin (CD62P) nor E-selectin (CD62E) by cells. Additional experiments performed neutralizing Abs specific IL-1alpha, IL-1beta, IL-6, TNF-alpha, respectively, excluded autocrine mechanism responsible up-regulation. virus-induced up-regulation dependent protein kinase C A, PI3K, p38 MAPK activity. Adhesion polymorphonuclear neutrophil granulocytes (PMN) ICAM-1-dependent adhesion rate PMN cocultured Furthermore, adhesiveness resulted transmigration PMN. Our vitro data suggest infection might contribute accumulation into bronchoalveolar space.