Springer, Jochen, Geppetti, Pierangelo, Fischer, Axel and Groneberg, David A. (2003) Calcitonin gene-related peptide as inflammatory mediator. Pulmonary Pharmacology & Therapeutics, 16 (3). pp. 121-130. ISSN 1522-9629
Full text not available from this repository.Abstract
Sensory 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 β-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.
Item Type: | Article |
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Faculty \ School: | Faculty of Medicine and Health Sciences > Norwich Medical School |
UEA Research Groups: | Faculty of Medicine and Health Sciences > Research Groups > Gastroenterology and Gut Biology |
Depositing User: | Rhiannon Harvey |
Date Deposited: | 09 Jun 2011 15:36 |
Last Modified: | 07 Mar 2023 15:30 |
URI: | https://ueaeprints.uea.ac.uk/id/eprint/32178 |
DOI: | 10.1016/S1094-5539(03)00049-X |
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