Purpose of review
The discovery that a number of transient receptor potential (TRP) channels are expressed in a subpopulation of primary sensory neurons innervating the upper and lower airways as well as in nonneuronal cells in the airways and lungs has initiated a quest for the understanding of their role in the physiology and pathophysiology of the respiratory tract.
Various members of the TRP vanilloid subfamily (TRPV1, TRPV4) and the TRP ankyrin 1 (TRPA1), because of their localization in peptidergic sensory neurons, promote airway neurogenic inflammation. In particular, TRPA1, which is gated by oxidative and nitrative stress byproducts, has been found to mediate inflammatory responses produced by an unprecedented series of toxic and irritant agents produced by air pollution, contained in cigarette smoke, and produced by accidental events at the workplace. The observation that reactive molecules endogenously produced in the airways/lungs of asthma, work-related asthma, and chronic obstructive pulmonary disease target TRPA1 underscores the primary role of the TRPA1 channel in these conditions.
Identification of TRP channels, and especially TRPA1, as major targets of oxidative/nitrative stress and a variety of irritant environmental agents supports the hypothesis that neurogenic inflammation plays an important role in work-related inflammatory diseases and that antagonists for such channels may be novel therapeutic options for the treatment of these diseases.