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Published ahead of print on April 3, 2003, doi:10.1165/rcmb.2003-0035OC

Am. J. Respir. Cell Mol. Biol., Volume 29, Number 3, September 2003, 314-320

A more recent version of this article appeared on September 1, 2003
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Submitted on February 4, 2003
Revised on April 2, 2003

Role of prostaglandin I2 in airway remodeling induced by repeated allergen challenge in mice

Koichi Nagao1, Hiroyuki Tanaka1, Masato Komai1, Taisei Masuda1, Shuh Narumiya2, and Hiroichi Nagai1*

1 Department of Pharmacology, Gifu Pharmaceutical University, Gifu, Gifu, Japan, 2 Department of Pharmacology, Kyoto University Faculty of Medicine, Kyoto, Kyoto, Japan

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

Recently, we demonstrated that PGI2 has a regulatory role in allergic responses through the receptor, IP; however, the role of PGI2 in airway remodeling associated with chronic airway inflammation has not been elucidated. In the present study, we examined the role of PGI2 in allergen-induced airway remodeling using IP gene deficient mice. Mice were sensitized to ovalbumin (OA) with alum, and exposed daily for 3 weeks to aerosolized OA. Twenty-four h after the final antigen inhalation, bronchoalveolar lavage (BAL), biochemical and histopathological examinations were carried out. In wild-type mice, prolonged allergen exposure in sensitized animals induced the increases in the numbers of inflammatory leukocytes (including eosinophils and lymphocytes), levels of T helper type 2 (Th2) cytokines (IL-4, IL-5 and IL-13), levels of OA-specific IgE and IgG1 in serum, and amount of hydroxyproline in the right lungs associated with transforming growth factor-{beta} 1 levels in BAL fluid. Moreover, goblet cell hyperplasia and subepithelial fibrosis were also appreciated after repeated allergen challenge. In contrast, the disruption of IP gene significantly augmented all these parameters. These findings suggest that PGI2 has a regulatory role in allergen-induced airway remodeling as well as airway eosinophilic inflammation, Th2 cytokine production and IgE production, and that a PGI2 agonist is a therapeutic approach for the treatment of airway remodeling in allergic asthma.




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