Lipoxin A4 regulates PM2.5-induced severe allergic asthma in mice via the Th1/Th2 balance of group 2 innate lymphoid cells.

BACKGROUND

Urban particulate matter (PM) contributes to the increasing number of people with asthma, which is closely related to the development of industrialization. Especially, PM with an aerodynamic diameter of <2.5 µm (PM2.5) enhances the risk of damaging respiratory organs. It has reported that PM2.5-induced pathological changes could be considered as a remarkable molecular mechanism of PM2.5-mediated cytotoxicity in respiratory disease and even lung cancer.

METHODS

In this study, we have investigated the effects of PM2.5 on ovalbumin (OVA)-induced asthma mice and the therapeutic effect of Lipoxin A4 (LXA) on improving the poor pathology.

RESULTS

The exposure of PM2.5 showed that both cytokines of T helper-2 (Th2) cells and transcription factors of group 2 innate lymphoid cells (ILC2s) were significantly increased, and inflammatory cell infiltration occurred in lung tissue. The LXA was used to treat asthma, which was an effective option in reducing inflammatory cytokines and relieving pathological symptoms, probably by regulating the Th1/Th2 balance.

CONCLUSIONS

These results suggest that PM2.5-induced inflammation plays a key role in the progression of asthma mice. In addition, LXA has a significant therapeutic effect on asthma, which indicates the direction for the treatment of asthma related inflammatory diseases.