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pubmed-article:12749828pubmed:abstractTextSensory neuropeptides have been proposed to play a key role in the pathogenesis of a number of respiratory diseases such as asthma, chronic obstructive pulmonary disease or chronic cough. Next to prominent neuropeptides such as tachykinins or vasoactive intestinal polypeptide (VIP), calcitonin gene-related peptide (CGRP) has long been suggested to participate in airway physiology and pathophysiology. CGRP is a 37 amino-acid peptide which is expressed by nerve fibers projecting to the airways and by pulmonary neuroendocrine cells. The most prominent effects of CGRP in the airways are vasodilatation and in a few instances bronchoconstriction. A further pulmonary effect of CGRP is the induction of eosinophil migration and the stimulation of beta-integrin-mediated T cell adhesion to fibronectin at the site of inflammation. By contrast, CGRP inhibits macrophage secretion and the capacity of macrophages to activate T-cells, indicating a potential anti-inflammatory effect. Due to the complex pulmonary effects of CGRP with bronchoconstriction and vasodilatation and diverse immunomodulatory actions, potential anti-asthma drugs based on this peptide have not been established so far. However, targeting the effects of CGRP may be of value for future strategies in nerve modulation.lld:pubmed
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pubmed-article:12749828pubmed:pagination121-30lld:pubmed
pubmed-article:12749828pubmed:dateRevised2006-11-15lld:pubmed
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pubmed-article:12749828pubmed:year2003lld:pubmed
pubmed-article:12749828pubmed:articleTitleCalcitonin gene-related peptide as inflammatory mediator.lld:pubmed
pubmed-article:12749828pubmed:affiliationDivision of Allergy Research, Department of Pediatric Pneumology and Immunology, Charité Campus-Virchow, Humboldt-University Berlin, 13353 Berlin, Germany.lld:pubmed
pubmed-article:12749828pubmed:publicationTypeJournal Articlelld:pubmed
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pubmed-article:12749828pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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