The Journal of Experimental Medicine
Avanti Polar Lipids, Inc.
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents

This Article
Right arrow Full Text
Right arrow Full Text (PDF, 169K)
Right arrow PPT slides of all figures
Right arrow Alert me when this article is cited
Right arrow Citation Map
Services
Right arrow Email this article
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new content in the JEM
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Akimoto, T.
Right arrow Articles by Akira, S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Akimoto, T.
Right arrow Articles by Akira, S.
Social Bookmarking
 Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Facebook   Add to Reddit   Add to Technorati   Add to Twitter  
What's this?
© The Rockefeller University Press, 0022-1007/1998/5/1537/ $5.00
The Journal of Experimental Medicine, Volume 187, Number 9, May 4, 1998 1537-1542


Brief Definitive Reports

Abrogation of Bronchial Eosinophilic Inflammation and Airway Hyperreactivity in Signal Transducers and Activators of Transcription (STAT)6-deficient Mice

Toshihiko Akimoto*, Fumio Numata*, Misato Tamura*, Yoshimi Takata*, Noriko Higashida*, Tohru Takashi*, Kiyoshi Takeda{ddagger}, and Shizuo Akira{ddagger}

From the * New Product Research Laboratories IV, Daiichi Pharmaceutical Co., Ltd., 1-16-13 Kitakasai, Edogawa, Tokyo 134, Japan; and the {ddagger} Department of Biochemistry, Hyogo College of Medicine, 1-1 Mukogawa, Nishinomiya, Hyogo 663, Japan

Signal transducers and activators of transcription 6 (STAT6) is essential for interleukin 4–mediated responses, including class switching to IgE and induction of type 2 T helper cells. To investigate the role of STAT6 in allergic asthma in vivo, we developed a murine model of allergen-induced airway inflammation. Repeated exposure of actively immunized C57BL/6 mice to ovalbumin (OVA) aerosol increased the level of serum IgE, the number of eosinophils in bronchoalveolar lavage (BAL) fluid, and airway reactivity. Histological analysis revealed peribronchial inflammation with pulmonary eosinophilia in OVA-treated mice. In STAT6-deficient (STAT6–/–) C57BL/6 mice treated in the same fashion, there were no eosinophilia in BAL and significantly less peribronchial inflammation than in wild-type mice. Moreover STAT6–/– mice had much less airway reactivity than wild-type mice. These findings suggest that STAT6 plays a crucial role in the pathogenesis of allergen-induced airway inflammation.


Address correspondence to Toshihiko Akimoto, New Product Research Laboratories IV, Daiichi Pharmaceutical Co., Ltd., 1-16-13 Kitakasai, Edogawa, Tokyo 134-8630, Japan. Phone: 81-3-3680-0151; Fax: 81-3-5696-4264; E-mail: jde03537{at}niftyserve.or.jp


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Facebook Facebook   Add to Reddit Reddit   Add to Technorati Technorati   Add to Twitter Twitter    What's this?




  Home | Help | Feedback | Subscriptions | Archive | Search
TABLE OF CONTENTS