Adhesion molecule expression on epithelial cells infected with respiratory syncytial virus

被引:43
|
作者
Wang, SZ
Hallsworth, PG
Dowling, KD
Alpers, JH
Bowden, JJ
Forsyth, KD
机构
[1] Flinders Univ S Australia, Flinders Med Ctr, Dept Paediat, Adelaide, SA 5001, Australia
[2] Flinders Univ S Australia, Flinders Med Ctr, Dept Microbiol, Adelaide, SA 5001, Australia
[3] Flinders Univ S Australia, Flinders Med Ctr, Dept Pathol, Adelaide, SA 5001, Australia
[4] Flinders Univ S Australia, Flinders Med Ctr, Dept Resp Med, Adelaide, SA 5001, Australia
关键词
adhesion molecule; epithelial cell; infection; respiratory syncytial virus;
D O I
10.1034/j.1399-3003.2000.15b23.x
中图分类号
R56 [呼吸系及胸部疾病];
学科分类号
摘要
Respiratory epithelium is both a target and an effector of airway inflammation. Adhesion molecules on epithelium play an important role in a variety of airway diseases. Respiratory syncytial virus (RSV) is the most important pathogen for airway diseases in infants. The expression of adhesion molecules on epithelium in RSV infection, however, is unclear. The expression of selected adhesion molecules and major histocompatibility complex (MHC) class I and II antigens on a human alveolar type II epithelial cell line (A549) infected with RSV was investigated by means of pow cytometry and immunocytochemistry. The results showed that intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) were expressed on A549 cells at a low level, E-cadherin and MHC class I antigen were constitutively expressed on the cells, RSV infection of A549 cells significantly upregulated the expression of ICAM-1, VCAM-1 and MHC class I and II antigens on these cells. RSV infection also altered the expression of E-cadherin on A549 cells, Immunostaining showed that E-cadherin was mainly upregulated around or in RSV-induced giant cells. These data suggest that respiratory syncytial virus infection of respiratory epithelial cells enhances the expression of adhesion molecules and major histocompatiblity. complex antigens, These changes may play an important role in the pathophysiology of respiratory syncytial virus disease.
引用
收藏
页码:358 / 366
页数:9
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