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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Article info
Publication history
Received:
May 15,
2013
Identification
Copyright
© 2013 Published by Elsevier Inc.
