Interferon-beta augments eosinophil adhesion-inducing activity of endothelial cells.

Viral infections induce exacerbations of asthma. One of the earliest host responses to viral infections is the production of innate cytokines including type I interferons (IFNs), such as IFN-beta, which may act to modify airway inflammation. The objective of the present study was to investigate whether IFN-beta modifies the eosinophil adhesion-inducing activity of endothelial cells. Human umbilical vein endothelial cells (HUVECs) were stimulated with IFN-beta for 24 h in the presence or absence of tumour necrosis factor (TNF)-alpha. Eosinophils were isolated from the peripheral blood of healthy volunteers. The ability of the IFN-beta-stimulated HUVEC monolayers to induce eosinophil adhesion was assessed according to the eosinophil peroxidase assay. Eosinophil adhesion to HUVECs was significantly augmented by IFN-beta in the presence of TNF-alpha but not in its absence. The augmented adhesion was inhibited by anti-alpha(4) integrin monoclonal antibody (mAb) or anti-beta(2) integrin mAb. IFN-beta significantly enhanced the expression of vascular cell adhesion molecule-1 and intercellular adhesion molecule-1 on HUVECs in the presence of TNF-alpha. Interferon-beta can augment the adhesiveness of endothelial cells to eosinophils, mainly through the expression of vascular cell adhesion molecule-1 and intercellular adhesion molecule-1. This action of interferon-beta may contribute to the intensification of airway inflammation in asthma that is associated with exacerbations induced by viral infections.