Abstract

Introduction. The involvement of macrophages in the realization of oxidative / halogenating stress andthe role of macrophage populations in maintaining the balance of Th1/Th2 cytokines in patients with asthma with osmotic types of bronchial hyperresponsiveness has not been sufficiently studied.Aim. To study the role of macrophages, myeloperoxidase (MPO), IL-12, IL-13 in the formation of the bronchial response to the hyperosmolar trigger in patients with asthma.Materials and methods. The object of the study was asthma patients (n=35). The level of asthma control (Asthma Control Test, points), cellular composition (%) and MPO (pixel) of induced sputum (IS), bronchial response (ΔFEV1IHS, %) after 3-minute ultrasonic inhalation of hypertonic (4.5% NaCl) solution (IHS) were assessed. Before and after the IHS test, exhaled air condensate was collected, in which the concentration of IL-12, IL-12 (pg/mL) was determined.Results. Patients with asthma did not control the disease, ACT was 14 (11; 16.5) points. Group 1 (n=15) included individuals with bronchial hyperresponsiveness to the IHS, group 2 (n=20) included patients with lack of it (ΔFEV1IHS -19.8±1.9 and 1.43±0.72%, respectively, p<0.001). Baseline FEV1 in groups 1 and 2 was 89.5±2.8 and 93.7±2.3%, respectively (p>0.05). The percentage of sputum macrophages in group 1 was lower (40 [15.95; 50.75]%), and the average cytochemical coefficient in phagocytes was higher (141.4±9.7) than in group 2 (50 [42.5; 63.6]; p=0.039 and 98.8±12.3; p=0.013, respectively). IL-12 expression was to be more significant than IL-13 expression in the initiation of airway inflammation and hyperresponsiveness to hyperosmolar stimulus.Conclusion. The lower concentration of macrophages in the bronchi of asthma patients with airway hyperresponsiveness to hyperosmolar stimulus is most likely due to an increase in the secretory function of cells. A high level of MPO activity in these patients depended on the peroxidase function of secreting macrophages, was associated with M1 polarization of macrophages, and indicated a Th1 immune response associated with the participation of IL-12 in the regulation of airway hyperresponsiveness to a hypertonic trigger.

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