Airborne particulate matter as drivers of airway inflammation in T2-endotype asthma

The paper presents the modern concept of airway inflammation formation in T2 endotype asthma under the exposure to ambient air particulate matter (PM). It was shown that PM exposure leads to disruption of the epithelial barrier integrity and epithelial cells damage, triggering the alarmins production with subsequent activation of dendritic cells, Th2 lymphocytes, and/or type 2 innate lymphoid cells. The role of PM in eosinophilic inflammation in both allergic and non-allergic asthma phenotypes was highlighted. Moreover, evidence suggests that PM may modify the structure and activity of certain aeroallergens. Furthermore, a correlation was demonstrated between PM concentrations and asthma incidence. Prenatal PM exposure leads to increased risk for childhood asthma. An association was found between PM concentration and disease progression, exacerbation frequency, and emergency care visits. The results of experimental, epidemiological, and clinical data show the significant role of PM in driving airway inflammation in the T2-endotype asthma. This highlights the need for further research to develop preventive strategies and novel therapeutic approaches.