Epigenetic regulation is involved in traffic-related PM_2.5 aggravating allergic airway inflammation in rats

Increasing fine particulate matter (PM_2.5) and epigenetic modifications are closely associated with the pathogenesis of asthma, but the definite mechanism remains unclear. The traffic-related PM_2.5 exposure aggravated pulmonary inflammation and changed the methylation level of interferon gamma (Ifng) and interleukin (Il)4 genes, and then altered levels of affiliated cytokines of IFN-γ and IL-4 in rats with allergic airway inflammation. It also increased the level of miR146a and decreased the level of miR31. In addition, transcription factors of nuclear factor kappa B (NF-κB) and signal transducer and activator of transcription 6 (Stat6) rose; forkhead box P3 (Foxp3) and signal transducer and activator of transcription 4 (Stat4) lowered. The traffic-related PM_2.5 altered epigenetic modifications in allergic airway inflammation of rats leading to inflammation exacerbation through impaired regulatory T (Treg) cells function and T-helper type 1 (Th1)/Th2 cells imbalance, which provided a new target for the treatment and control of asthma.