Wang S Z, Hallsworth P G, Dowling K D, Alpers J H, Bowden J J, Forsyth K D
Dept of Paediatrics, Flinders Medical Centre, Flinders University, Adelaide, South Australia, Australia.
Eur Respir J. 2000 Feb;15(2):358-66. doi: 10.1034/j.1399-3003.2000.15b23.x.
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 flow 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 histocompatibility complex antigens. These changes may play an important role in the pathophysiology of respiratory syncytial virus disease.
呼吸道上皮既是气道炎症的靶标，也是效应器。上皮细胞上的黏附分子在多种气道疾病中起重要作用。呼吸道合胞病毒（RSV）是婴儿气道疾病最重要的病原体。然而，RSV感染时上皮细胞上黏附分子的表达尚不清楚。采用流式细胞术和免疫细胞化学方法，研究了感染RSV的人肺泡II型上皮细胞系（A549）上选定黏附分子以及主要组织相容性复合体（MHC）I类和II类抗原的表达。结果显示，细胞间黏附分子-1（ICAM-1）和血管细胞黏附分子-1（VCAM-1）在A549细胞上低水平表达。E-钙黏蛋白和MHC I类抗原在细胞上组成性表达。A549细胞感染RSV后，这些细胞上ICAM-1、VCAM-1以及MHC I类和II类抗原的表达显著上调。RSV感染还改变了A549细胞上E-钙黏蛋白的表达。免疫染色显示，E-钙黏蛋白主要在RSV诱导的巨细胞周围或内部上调。这些数据表明，呼吸道上皮细胞感染呼吸道合胞病毒会增强黏附分子和主要组织相容性复合体抗原的表达。这些变化可能在呼吸道合胞病毒疾病的病理生理学中起重要作用。
