ICAM-1 expression and low-molecular-weight G-protein activation of human bronchial epithelial cells (A549) infected with RSV.

The airway epithelial cell of the lower respiratory tract is the primary host target cell for respiratory syncytial virus (RSV) infection. To estimate whether infected epithelial cells contribute to the inflammatory host response observed during the acute infection phase we analyzed the cell surface expression of intercellular adhesion molecule-1 (ICAM-1, CD54) on human bronchial epithelial cells (A549) following RSV infection and cytokine priming. The epithelial cells constitutively expressed ICAM-1. The ICAM-1 surface expression was significantly up-regulated up to 72 h post RSV infection. In addition, cytokine priming with tumor necrosis factor alpha (TNF-alpha), interferon-gammma (IFN-gamma), or interleukin-1 alpha/beta (IL-1alpha/beta) induced an enhanced ICAM-1 expression on noninfected as well as on RSV-infected epithelial cells. As early as 24 h post RSV infection and cytokine priming, respectively, the maximum of ICAM-1-expressing cells was observed. In contrast, the maximal ICAM-1 up-regulation per cell was measured 24 h later, e.g., after 48 h of culture. Cytokine priming with IL-3, IL-6, granulocyte-macrophage colony-stimulating factor (GM-CSF), or granulocyte colony-stimulating factor (G-CSF) did not lead to a significant increase of ICAM-1 expression either on RSV-infected or on noninfected A549 cells up to 72 h of culture time. Performed signal transduction experiments, e.g. [alpha-32P]GTP-binding blot analysis, revealed that low-molecular-weight GTP-binding proteins possess an enhanced GTP-binding capacity in RSV-infected A549 cells.