Interferon-β augments eosinophil adhesion-inducing activity of endothelial cells

Abstract

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-β, which may act to modify airway inflammation. The objective of the present study was to investigate whether IFN-β modifies the eosinophil adhesion-inducing activity of endothelial cells. Human umbilical vein endothelial cells (HUVECs) were stimulated with IFN-β for 24 h in the presence or absence of tumour necrosis factor (TNF)-α. Eosinophils were isolated from the peripheral blood of healthy volunteers. The ability of the IFN-β-stimulated HUVEC monolayers to induce eosinophil adhesion was assessed according to the eosinophil peroxidase assay. Eosinophil adhesion to HUVECs was significantly augmented by IFN-β in the presence of TNF-α but not in its absence. The augmented adhesion was inhibited by anti-α4 integrin monoclonal antibody (mAb) or anti-β2 integrin mAb. IFN-β significantly enhanced the expression of vascular cell adhesion molecule-1 and intercellular adhesion molecule-1 on HUVECs in the presence of TNF-α. Interferon-β 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-β may contribute to the intensification of airway inflammation in asthma that is associated with exacerbations induced by viral infections. Copyright©ERS Journals Ltd 2008.