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Published ahead of print on February 19, 2004, doi:10.1165/rcmb.2003-0305OC

Am. J. Respir. Cell Mol. Biol., Volume 31, Number 1, July 2004, 62-68

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Submitted on August 20, 2003
Revised on February 19, 2004

Role of IL-5 and eosinophils in allergen-induced airway remodeling in mice

Hiroyuki Tanaka1, Masato Komai1, Koichi Nagao1, Masayuki Ishizaki1, Daisuke Kajiwara1, Kiyoshi Takatsu2, Guy Delespesse3, and Hiroichi Nagai1*

1 Department of Pharmacology, Gifu Pharmaceutical University, Gifu, Gifu, Japan, 2 Department of Immunology, The Institute of Medical Science, University of Tokyo, Tokyo, Japan, 3 Allergy Research Laboratory, Centre de Recherche du Centre Hospitalier Universite de Montreal (CHUM), Notre-Dame Hospital, University of Montreal, Montreal, Quebec, Canada

* To whom correspondence should be addressed. E-mail: nagai{at}gifu-pu.ac.jp.

Asthma is a chronic inflammatory disease characterized by variable bronchial obstruction, hyperresponsiveness and by tissue damage known as airway remodeling. In the present study we demonstrate that IL-5 plays an obligatory role in the airway remodeling observed in experimental asthma. BALB/c mice sensitized by intraperitoneal injections of OVA and exposed daily to aerosol of OVA for up to 3 wks, develop eosinophilic infiltration of the bronchi and subepithelial and peribronchial fibrosis. The lesions are associated with increased amounts of hydroxyproline in the lungs and elevated levels of eosinophils and TGF-{beta}1 in the bronchoalveolar lavage fluid. After one week of allergen challenge, TGF-{beta} is mainly produced by eosinophils accumulated in the peribronchial and perivascular lesions. At a later stage of the disease, the main source of TGF-{beta} is myofibroblasts, identified by {alpha}-smooth muscle actin mAB. We show that all these lesions, including fibrosis, are abolished in sensitized and allergen exposed IL-5 receptor null mice, whereas they are markedly accentuated in IL-5 transgenic animals. More importantly, treatment of wild type mice with neutralizing anti-IL-5 antibody, administered before each allergen challenge, almost completely prevented subepithelial and peribronchial fibrosis. These findings demonstrated that eosinophils are involved in allergen-induced subepithelial and peribronchial fibrosis probably by producing a fibrogenic factor, TGF-{beta}1.




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