title: Interferon-beta 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-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.
authors.affiliation: Dept of Respiratory Medicine, Saitama Medical University, Saitama, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Kobayashi
authors.forename: Y
authors.initials: Y
authors.lastname: Takaku
authors.forename: A
authors.initials: A
authors.lastname: Yokote
authors.forename: H
authors.initials: H
authors.lastname: Miyazawa
authors.forename: T
authors.initials: T
authors.lastname: Soma
authors.forename: K
authors.initials: K
authors.lastname: Hagiwara
authors.forename: M
authors.initials: M
authors.lastname: Kanazawa
authors.forename: M
authors.initials: M
authors.lastname: Nagata
mesh_terms: D018821:CD18 Antigens / Q000378:metabolism; D002448:Cell Adhesion; D002460:Cell Line; D042783:Endothelial Cells / Q000378:metabolism*; D004730:Endothelium, Vascular / Q000166:cytology*; D004804:Eosinophils / Q000378:metabolism*; D006801:Humans; D007249:Inflammation; D039441:Integrin alpha4 / Q000378:metabolism; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D016899:Interferon-beta / Q000378:metabolism*; D008024:Ligands; D008954:Models, Biological; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D019010:Vascular Cell Adhesion Molecule-1 / Q000378:metabolism
chemical_list: D018821:CD18 Antigens; D008024:Ligands; D014409:Tumor Necrosis Factor-alpha; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D039441:Integrin alpha4; D016899:Interferon-beta