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Published ahead of print on May 4, 2006, doi:10.1165/rcmb.2005-0452OC

Am. J. Respir. Cell Mol. Biol., Volume 35, Number 3, September 2006, 366-377

A more recent version of this article appeared on September 1, 2006
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Submitted on December 8, 2005
Revised on May 4, 2006

Pirfenidone Modulates Airway Responsiveness, Inflammation and Remodeling After Repeated Challenge

Atsushi Hirano1, Arihiko Kanehiro2, Katsuichiro Ono1, Wataru Ito1, Akio Yoshida1, Chiharu Okada1, Hiromi Nakashima1, Yasushi Tanimoto1, Mikio Kataoka1, Erwin W Gelfand3*, and Mitsune Tanimoto1

1 Department of Hematology, Oncology and Respiratory Medicine, Okayama University Graduate School of Medicine and Dentistry, Okayama, Japan, 2 Department of Hematology, Oncology and Respiratory Medicine, Okayama University Graduate School of Medicine and Dentistry, Okayama, Japan; Program in Cell Biology, Department of Pediatrics, National Jewish Medical and Research Center, Denver, CO, USA, 3 Program in Cell Biology, Department of Pediatrics, National Jewish Medical and Research Center, Denver, CO, USA

* To whom correspondence should be addressed. E-mail: gelfande{at}njc.org.

We investigated the therapeutic potential of a newly developed anti-fibrotic agent, pirfenidone, to regulate airway remodeling, as well as the development of allergic airway inflammation and airway hyperresponsiveness (AHR) following chronic allergen challenge. Administration of pirfenidone after sensitization but during the period of OVA challenge significantly prevented development of AHR, as well as eosinophil and lymphocyte accumulation in the airways. IL-4, IL-5, and IL-13 levels in bronchoalveolar lavage (BAL) fluid and OVA-specific serum IgE antibody levels were also significantly reduced. Further, treatment with pirfenidone significantly reduced transforming growth factor-beta1 (TGF-{beta}1) and platelet-derived growth factor (PDGF) levels in BAL fluid. In addition, the expression of TGF-{beta}1, and the development of goblet cell hyperplasia, subepithelial collagenization and the increases in contractile elements in the lung were reduced by pirfenidone. These data indicate that pirfenidone may play an important role in the treatment of asthma and has the potential reduce or prevent airway remodeling.




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