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

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

CORRESPONDENCE: M. Nagata, Dept of Respiratory Medicine, Saitama Medical University, Morohongo 38, Moroyama, Iruma, Saitama 350-0495, Japan. Fax: 81 492761319. E-mail: favre4mn{at}saitama-med.ac.jp

Keywords: Asthma, endothelial cells, eosinophilic airway inflammation, viral infection

Received: May 16, 2007
Accepted June 12, 2008

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)-. 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- but not in its absence. The augmented adhesion was inhibited by anti-₄ 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-.

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.