BACKGROUND: It is now well established that allergens induce eosinophilic inflammation in T2 endotype of asthma. However, much less is known about the role of non-specific factors (suspended particles in the atmospheric air-PM).
AIMS: To define eosinophilic inflammation on the basis of several biomarkers in T2 endotype of asthma exposed to PM.
MATERIALS AND METHODS: We studied 61 patients with T2 endotype of asthma (ages 18-65). Group 1 included 34 patients with allergic asthma and group 2 included 27 patients with non-allergic asthma. Moreover, 30 healthy matched controls without asthma and other allergic diseases were enrolled the study. We performed clinical examination and allergy testing. Additionally, serum levels of IL-33, IL-25, IL-4, IL-5, IL-13, DPP4 (multiplex assay) and periostin (ELISA) were evaluated. The analyses of annual concentration average (Avr) and maximal annual concentration (MaxAvr) average of PM2.5 and PM10 in Kazan were carried out using the database of the Center for Hygiene and Epidemiology in the Republic of Tatarstan for 2014-2020. Statistical analyseswere performedusing the R statistical software (version 4.0.5). The study was funded by RFBR (project number 19-05-50094).
RESULTS: We detected increased blood eosinophil count and IL-5 levels in asthma patients. High levels of total IgE (p=0.0001), that correlated with IL-4 levels were observed only in patients with allergic asthma (rS=0.38; р=0.045). Moreover, elevated IL-25 levels were found in patients with allergic asthma (p=0.009). No significant differences in IL-13 levels in patient with asthma were found. Regression analysis revealed that the PM2.5Avr increase by 1 mcg/m3 results in the growth of IL-33 and IL-25 levels, but the PM10Avr increase raises the IL-25 levels only in patients with non-allergic asthma. No significant increase in IL-25 and IL-33 levels under the exposure to PM2.5Avr and PM 10Avr was detected in patients with allergic asthma.
CONCLUSIONS: The results of this study indicate the pivotal role of fine suspended particles in the development and maintenance of eosinophilic inflammation in patients with non-allergic asthma.