| First Author | Aoki-Nagase T | Year | 2002 |
| Journal | Am J Physiol Lung Cell Mol Physiol | Volume | 283 |
| Issue | 5 | Pages | L963-70 |
| PubMed ID | 12376349 | Mgi Jnum | J:80218 |
| Mgi Id | MGI:2445283 | Doi | 10.1152/ajplung.00130.2002 |
| Citation | Aoki-Nagase T, et al. (2002) Attenuation of antigen-induced airway hyperresponsiveness in CGRP-deficient mice. Am J Physiol Lung Cell Mol Physiol 283(5):L963-70 |
| abstractText | Bronchial hyperresponsiveness and eosinophilia are major characteristics of asthma. Calcitonin gene-related peptide (CGRP) is a neuropeptide that has various biological actions. In the present 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 with the sensitized wild-type mice. Antigen challenge induced eosinophil infiltration in bronchoalveolar lavage fluid, whereas no differences were observed between the wild-type and CGRP-mutant mice. Antigen-induced increases in cysteinyl leukotriene production in the lung were 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. |
