Abstract| Volume 177, ISSUE 1, P46, August 2013

FGF1 and 18 increase TRPV1 and TRPA1 responses in sensory C-fibers

      Allergic asthma is an inflammatory disease that is associated with airway hyperreactivity (AHR). AHR is characterized by cough, dyspnea and an enhanced sputum production in response to many environmental stimuli such as cold air, cigarette smoke and ozone. Evidence has been provided that sensory neurons, especially the unmyelinated C-fibers, might contribute to AHR. Airway innervating C-fibers express transient receptor potential vanilloid 1 (TRPV1) and transient receptor potential ankyrin 1 (TRPA1). TRPV1 and TRPA1 are cation channels that can be activated by most of those irritants which cause AHR-related asthma attacks. Therefore, it is speculated that TRP channels are key players in the pathogenesis of AHR. However, the mechanisms by which TRPV1 and TRPA1 are regulated in asthma are unclear. At least 22 fibroblast growth factors (FGFs) have been identified which activate FGF receptors. FGFs are located in epithelial and endothelial basement membranes, and are upregulated in the airways in allergic asthma. The aim of this study is to investigate if FGFs can regulate TRPV1 and TRPA1 sensitivity.
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