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Published online before print March 1, 2006, 10.1183/09031936.06.00107004
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Eur Respir J 2006; 27:726-734
Copyright ©ERS Journals Ltd 2006

Role of macrophage migration inhibitory factor in ovalbumin-induced airway inflammation in rats

M. Kobayashi1, Y. Nasuhara1, A. Kamachi2, Y. Tanino1, T. Betsuyaku1, E. Yamaguchi3, J. Nishihira4 and M. Nishimura1

1 First Dept of Medicine and, 4 Central Research Institute, Hokkaido University School of Medicine, Sapporo, and 2 Dept of Respiratory Medicine, Oji Municipal General Hospital, Tomakomai, and 3 Division of Respiratory Medical and Allergy Dept of Internal Medicine, Aichi Medical University School of Medicine, Aichi, Japan.

CORRESPONDENCE: Y. Nasuhara, First Dept of Medicine, Hokkaido University School of Medicine, North 15 West 7, Kita-ku, Sapporo 060-8638, Japan. Fax: 81 117067899. E-mail: nasuhara{at}med.hokudai.ac.jp

Keywords: Airway hyperresponsiveness, airway inflammation, asthma, eosinophil, macrophage migration inhibitory factor, ovalbumin

Received: September 14, 2004
Accepted January 5, 2006

Macrophage migration inhibitory factor (MIF) is a pro-inflammatory cytokine that reportedly counteracts the anti-inflammatory effect of endogenous glucocorticoids. There have only been a few reports that demonstrate a potential link between MIF and bronchial asthma. In an attempt to further clarify the precise role of MIF in asthma, the present authors examined the effect of anti-MIF antibody (Ab) on airway inflammation and airway hyperresponsiveness in an ovalbumin-immunised rat asthma model.

Actively immunised Brown Norway rats received ovalbumin inhalation with or without treatment of anti-MIF Ab. The levels of MIF in bronchoalveolar lavage fluid were significantly elevated after the ovalbumin challenge.

An immunohistochemical study revealed positive immunostaining for MIF in bronchial epithelium, even in nonsensitised rats, and the MIF staining in bronchial epithelium was enhanced after the ovalbumin challenge. Anti-MIF Ab significantly decreased the number of total cells, neutrophils and eosinophils in the bronchoalveolar lavage fluid of the ovalbumin-challenged rats, and also attenuated the ovalbumin-induced airway hyperresponsiveness to ovalbumin and methacholine. However, anti-MIF Ab did not affect the level of serum ovalbumin-specific IgE, suggesting that anti-MIF Ab did not suppress immunisation itself.

The results indicate that macrophage migration inhibitory factor plays a crucial role in airway inflammation and airway hyperresponsiveness in asthma.




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