Interferon- augments eosinophil adhesion-inducing activity of endothelial cells

¹ Dept of Respiratory Medicine, Saitama Medical University, Saitama, Japan

	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-, which may act to modify airway inflammation. The objective of this study was to investigate whether IFN- modifies the eosinophil adhesion-inducing activity of endothelial cells.

Human umbilical vein endothelial cells (HUVECs) were stimulated with IFN- for 24 h in the presence or absence of TNF-. Eosinophils were isolated from the peripheral blood of healthy volunteers. The ability of the IFN--stimulated HUVEC monolayers to induce eosinophil adhesion was assessed according to the eosinophil peroxidase assay.

Eosinophil adhesion to HUVECs was significantly augmented by IFN- not in the absence but in the presence of TNF-. The augmented adhesion was inhibited by anti-₄ integrin monoclonal antibody (mAb) or anti-₂ integrin mAb. IFN- significantly enhanced the expression of VCAM-1 and ICAM-1 on HUVECs in the presence of TNF-.

IFN- can augment the adhesiveness of endothelial cells to eosinophils, mainly through the expressions of VCAM-1 and ICAM-1. This action of IFN- may contribute to the intensification of airway inflammation in asthma that is associated with exacerbations induced by viral infections.