Adhesion molecule expression on epithelial cells infected with respiratory syncytial virus

Eur Respir J. 2000 Feb;15(2):358-66. doi: 10.1034/j.1399-3003.2000.15b23.x.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Adhesion Molecules / biosynthesis*
  • Epithelial Cells
  • Flow Cytometry
  • Histocompatibility Antigens Class I / biosynthesis
  • Histocompatibility Antigens Class II / biosynthesis
  • Humans
  • Immunohistochemistry
  • In Vitro Techniques
  • Respiratory Syncytial Virus Infections / immunology*
  • Respiratory Syncytial Virus Infections / metabolism
  • Tumor Cells, Cultured
  • Up-Regulation

Substances

  • Cell Adhesion Molecules
  • Histocompatibility Antigens Class I
  • Histocompatibility Antigens Class II