Interferon-alpha inhibits airway eosinophila and hyperresponsiveness in an animal asthma model
10.5415/apallergy.2012.2.4.256
- Author:
Yasuko KIKKAWA
1
;
Kumiya SUGIYAMA
;
Kazuki OBARA
;
Hirokuni HIRATA
;
Yasutsugu FUKUSHIMA
;
Masao TODA
;
Takeshi FUKUDA
Author Information
1. Department of Pulmonary Medicine and Clinical Immunology, Dokkyo Medical University, 880 Kita-kobayashi, Mibu, Tochigi 321-0293, Japan. sugiyama@dokkyomed.ac.jp
- Publication Type:Original Article
- Keywords:
Adhesion molecule;
Asthma;
Eosinophil;
Interferon-alpha;
Intercellular adhesion molecule-1;
Macrophage antigen-1
- MeSH:
Animals;
Asthma;
Churg-Strauss Syndrome;
Endothelial Cells;
Eosinophilia;
Eosinophils;
Guinea Pigs;
Hepatitis C, Chronic;
Human Umbilical Vein Endothelial Cells;
Humans;
Inflammation;
Intercellular Adhesion Molecule-1;
Interferon-alpha;
Interferons;
Interleukin-1;
Interleukin-1beta;
Lung;
Macrophages
- From:
Asia Pacific Allergy
2012;2(4):256-263
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND: Asthma is characterized by a chronic inflammatory process involving high numbers of inflammatory cells and mediators which have multiple inflammatory effects on the airway. Interferon (IFN)-alpha, which is used widely for treating chronic hepatitis C, is reported to have an effect on patients with Churg-Strauss syndrome. Therefore, it may also be suitable for patients with severe asthma. OBJECTIVE: We studied the effect of IFN-alpha on airway eosinophilia in a guinea pig model of asthma and the expression of adhesion molecules on human eosinophils and vascular endothelial cells. METHODS: After antigen challenge, airway hyperresponsiveness and airway eosinophilia were measured in a guinea pig asthma model with or without airway IFN-alpha administration. Expression of adhesion molecules on eosinophils and cultured human umbilical vein endothelial cells (HUVECs) was also evaluated with or without IFN-alpha. RESULTS: IFN-alpha inhibited eosinophil recruitment into the tracheal wall and improved airway hyperresponsiveness in sensitized guinea pigs. IFN-alpha also significantly suppressed IL-1 beta-induced intercellular adhesion molecule-1 (ICAM-1) expression on HUVECs. However, IFN-alpha did not suppress platelet-activating factor-induced macrophage antigen-1 expression on human eosinophils. IFN-alpha significantly inhibited eosinophil adhesion to IL-1 beta-induced HUVECs and migration through IL-1 beta induced HUVECs. CONCLUSION: The findings suggest that the modulation of ICAM-1 in lung with pre-existing inflammation following treatment with IFN-alpha may be a novel and selective treatment for control of chronic airway inflammation and hyperresponsiveness associated with asthma.
