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Am J Physiol Lung Cell Mol Physiol (June 21, 2002). doi:10.1152/ajplung.00130.2002
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Articles in PresS, published online ahead of print June 21, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00130.2002
Submitted on May 2, 2002
Accepted on June 17, 2002

Attenuation of antigen-induced airway hyperresponsiveness in CGRP-deficient mice

Tomoko Aoki-Nagase1, Takahide Nagase1*, Yoshio Oh-hashi2, Takayuki Shindo2, Yukiko Kurihara2, Yasuhiro Yamaguchi1, Hiroshi Yamamoto1, Tetsuji Tomita1, Eijiro Ohga1, Ryozo Nagai2, Hiroki Kurihara3, and Yasuyoshi Ouchi1

1 Department of Geriatric Medicine, University of Tokyo, Tokyo, Japan
2 Department of Cardiovascular Medicine, University of Tokyo, Tokyo, Japan
3 Department of Embryogenesis, Kumamoto University, Kumamoto, Japan

* To whom correspondence should be addressed. E-mail: takahide-tky{at}umin.ac.jp.

Bronchial hyperresponsiveness and eosinophilia are major characteristics of asthma. Calcitonin gene-related peptide (CGRP) is a neuropeptide that has various biological actions. In the current study, we questioned whether CGRP might have pathophysiological roles in airway hyperresponsiveness and eosinophilia in asthma. To determine the exact roles of endogenous CGRP in vivo, we chose to study antigen-induced airway responses using CGRP gene-disrupted mice. After ovalbumin sensitization and antigen challenge, we assessed airway responsiveness and measured proinflammatory mediators. In the sensitized CGRP gene-disrupted mice, antigen-induced bronchial hyperresponsiveness was significantly attenuated compared to the sensitized wild type mice. Antigen challenge induced eosinophil infiltration in bronchoalveolar lavage fluid (BALF), whereas no differences were observed between the wild type and CGRP mutant mice. Antigen-induced increases in cysteinyl leukotriene production in the lung was significantly reduced in the CGRP-disrupted mice. These findings suggest that CGRP could be involved in the antigen-induced airway hyperresponsiveness, but not eosinophil infiltration, in mice. The CGRP mutant mice may provide appropriate models to study molecular mechanisms underlying CGRP-related diseases.




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