Interaction between airway inflammation and gut microbiota dysbiosis caused by high temperatures (40 °C) and traffic-PM in mouse model.

Though epidemiological studies have shown that high temperatures and traffic-PM alone can increase the risk of asthma, there were not clear about their associated impact on asthma. This study investigated the combination effect of high temperatures (40 °C) and traffic-PM on asthma and molecular mechanism. BALB/c mice were treated with high temperature and traffic-PM. Firstly, airway hyperresponsiveness (AHR) was measured in vivo before lung histological analysis. The inflammation biomarkers of asthma were further analyzed to examine the role of oxidative stress, and TRPV1 and gut microbiota. Finally, we investigated whether vitamin E (Ve) and capsazepine (Czp) could protect against airway inflammation. Serum proteins, lung tissue cytokines, and proinflammatory factors with the high temperatures and traffic-PM treatment were markedly higher than those in the control groups. AHR indicated that lung function decreased after high temperatures and traffic-PM exposure. The lung histological assay demonstrated changes of airway. Our results showed that 40 °C and traffic-PM could aggravate airway inflammation, mainly through activation of oxidative stress and TRPV1. High temperature could change gut microbial community structure of asthma mice. Moreover, imbalance of Th1/Th2 exacerbated gut microbiota dysbiosis under high temperature. Hence, this study clarified asthma airway inflammation aggravated by environmental factors from the perspective of gut-lung axes providing novel theoretical basis for the treatment of asthma.