NEUROGENIC INFLAMMATION AND PECULIARITIES OF THE AUTONOMIC NERVOUS SYSTEM IN PATIENTS WITH BRONCHIAL ASTHMA DEPENDING ON THE SEVERITY AND PHENOTYPE OF THE DISEASE
Bronchial asthma (BA) is a heterogeneous disease characterized by chronic airway inflammation. The central link in the pathogenesis of the disease is the inflammatory process of the bronchial wall, the maintenance of which, along with allergens, infections and toxic agents, is facilitated by "neurogenic" inflammatory factors, and imbalance in the links of the autonomic nervous system. Vasointestinal peptide is involved in bronchodilation and substance P is currently considered as the main mediator of neurogenic inflammation, capable of causing such pathophysiological reactions as pain, mucosal edema, mucus hypersecretion, and bronchoconstriction. The research available to date does not fully reflect the mechanisms and degree of influence of the imbalance of the autonomic nervous system and neurogenic inflammation in patients with severe bronchial asthma. In this regard, the study of autonomic dysfunction and it’s connection with the clinical features of severe bronchial asthma is relevant and can contribute to the improvement of a personalized approach to the treatment of patients with asthma, which is of practical interest. Our study presents the results of the level of neuropeptides depending on the type of dysfunction of the autonomic nervous system, as well as the phenotype of bronchial asthma.