Several features of inflammation at the patients with atopic bronchial asthma when exposed to respiratory viruses

The modern interpretation of the pathogenesis bronchial asthma (ВА) emphasizes the role of systemic inflammation at the BA, since its development under the influence of specific (allergens) and non-specific factors leads to an imbalance of pro- and anti-inflammatory cytokines in the airways. It has been established that most exacerbations of BA occur due to the influence of respiratory viral infection (RVI). The process of inflammation in the airways with virus-induced exacerbations of BA depends on the type of respiratory virus, and also phenotype and endotype of BA at the patient. Based on in vitro and in vivo studies, the role of interleukin-33 (IL-33) in the pathogenesis exacerbation of atopic BA in the mouse model is described. The aim of our work is to determine the IL33 gene expression and study its role during development of atopic BA and its virus-induced exacerbation in humans. Material and methods. All volunteers included in the study were divided into groups: «BA», «BA+RVI», «RVI», «healthy donors». All study participants underwent clinical, laboratory, instrumental (spirometry), allergological, immunological examination (determination the expression mRNA of the IL33 gene in peripheral venous blood and identification the mRNA of respiratory viruses (RSV, RV, coronaviruses, influenza virus type A and B, metapnevmoviruses, adenoviruses, bokaviruses, parainfluenza viruses type 1, 2, 3, 4) in smears from the nasal cavity by RT-PCR). Results. In the «BA» and «BA+RVI» groups were observed the decrease FEV , increased the ACQ-7 (more than 1.5 points), the blood eosinophilia (P = 0.000002), which characterizes the uncontrolled course and exacerbation of atopic BA from volunteers. The highest level of the expression mRNA IL-33 was found at the «BA+RVI» group (P = 0.003), and in the absence of RVI in volunteers with exacerbation of atopic BA the level of IL-33 not differs from healthy donors. According to the results of our study the more severe course of atopic BA was observed in the season with a predominance of RSV infection in 2017 compared to 2016 according to ACQ-7 (P = 0.00004 and P = 0.0002) and FEV (P = 0.006 and P = 0.008), respectively. Conclusions. The results of the study provide additional evidence of the role of pro-inflammatory IL-33 in the pathogenesis of RVI and virus-induced exacerbations of atopic BA (most often RSV and RV). Identification of new mechanisms of virus-induced exacerbations of atopic BA can be used in the selection and development of personalized basic therapy of asthma. 1