Transient receptor potential ankyrin channel and brain-derived neurotrophic factor in the pathogenesis of asthma: ways of interaction

The complexity of the pathogenesis of bronchial asthma (BA) has been caused by the influence of the environmental, genetic and epigenetic factors that interact with each other and contribute to the development and exacerbation of this pathology. In recent years researchers have focused on the neurogenic component of the BA pathogenesis. The ankyrin receptor TRPA1(the transient receptor potential cation channel subfamily A member 1) is expressed in the sensory C-fibers of the lungs and activated by the cold, cigarette smoke, allergens and number of chemicals that are the triggers of BA. It triggers the influx of Ca 2+ into sensory neurons and activates the cascades responsible for the expression of the brain-derived neurotrophic factor (BDNF) gene. BDNF is involved in airway remodeling, enhances airway innervation and exacerbates airway hyperreactivity, and also maintains sensory hypersensitivity through a feedback loop. BDNF gene polymorphisms confer susceptibility to BA, with carriers of TRPA1 gene polymorphisms more sensitive to epigenetic modifications and may have strong BDNF expression in response to the stimuli. Despite the fact that the epigenetics of TRPA1 and BDNF in BA is under study, the epigenetic changes of TRPA1 and BDNF are well described in neurology, which may be interesting in the context of their interaction in BA, given the role of neuroimmune inflammation in the pathogenesis of this disease. The present review discusses the role and relationship of genetic and epigenetic changes induced by environmental factors initiating BA development, as well as role of TRPA1 and BDNF in this process.