title: Oxidative stress as activators of sensory nerves for cough.
abstract: Excessive activation of the cough reflex is a major clinical problem in respiratory diseases. The cough reflex is triggered by activation of nociceptive sensory nerve terminals innervating the airways by noxious stimuli. Oxidative stress is a noxious stimuli associated with inhalation of pollutants and inflammatory airway disease. Here, we discuss recent findings that oxidative stress, in particular downstream of mitochondrial dysfunction, evokes increased electrical activity in airway nociceptive sensory nerves. Mechanisms include activation of transient receptor potential (TRP) channels and protein kinase C. Such mechanisms may contribute to excessive cough reflexes in respiratory diseases.
authors.affiliation: Department of Molecular Pharmacology & Physiology, Morsani College of Medicine, University of South Florida, 12901 Bruce B Downs Blvd, Tampa, FL 33612, USA. Electronic address: ttaylorc@health.usf.edu.
authors.forename: Thomas E
authors.initials: TE
authors.lastname: Taylor-Clark
mesh_terms: D000818:Animals; D003371:Cough / Q000503:physiopathology*; D006801:Humans; D008928:Mitochondria / Q000378:metabolism; D018384:Oxidative Stress; D011984:Sensory Receptor Cells; D050051:Transient Receptor Potential Channels / Q000378:metabolism
chemical_list: D050051:Transient Receptor Potential Channels
keywords: Cough; Mitochondria; Nociception; Protein kinase C; Reactive oxygen species; TRP channel