Inflammation is one of the major adverse effects of fine particulate matter (PM_2.5) on the lung system; however, its mechanisms remain unclear. Rats were exposed to different concentrations of PM_2.5 to investigate the mechanism of short-term exposure-induced lung inflammation. The regulation of PI3K-Akt and DNA methyltransferase 3b (DNMT3b) was assessed by using a PI3K inhibitor and a DNA methyltransferase inhibitor. We found that PM_2.5 could decrease interferon-γ (IFN-γ) levels and increase interleukin 4 (IL-4), IL-5 and IL-13 levels in bronchoalveolar lavage fluid (BALF) to promote eosinophil infiltration and eventually lead to allergic pulmonary inflammation. Moreover, the CpG island methylation rate of the IFN-γ promoter and the protein expression of DNMT3b, PI3K and p-Akt were increased in lung tissues after PM_2.5 exposure. Both inhibitors reversed the CpG island hypermethylation of IFN-γ. In conclusion, in PM_2.5-induced lung injury, the activated PI3K-Akt pathway, via an increase in DNMT3b expression, is involved in CpG hypermethylation of the IFN-γ gene promoter.

炎症是细颗粒物（PM _2.5）对肺系统的主要不利影响之一；然而，其机制仍不清楚。大鼠暴露于不同浓度的 PM _2.5以研究短期暴露引起肺部炎症的机制。通过使用 PI3K 抑制剂和 DNA 甲基转移酶抑制剂评估 PI3K-Akt 和 DNA 甲基转移酶 3b (DNMT3b) 的调节。我们发现 PM _2.5可降低干扰素-γ（IFN-γ）水平，增加支气管肺泡灌洗液（BALF）中的白细胞介素4（IL-4）、IL-5和IL-13水平，促进嗜酸性粒细胞浸润，最终导致过敏性肺部炎症。_{此外，暴露于 PM 2.5}后，肺组织中 IFN-γ 启动子的 CpG 岛甲基化率和 DNMT3b、PI3K 和 p-Akt 的蛋白表达增加。两种抑制剂都逆转了 IFN-γ 的 CpG 岛高甲基化。总之，在 PM _2.5诱导的肺损伤中，激活的 PI3K-Akt 通路通过增加 DNMT3b 表达，参与了 IFN-γ 基因启动子的 CpG 高甲基化。