PM2.5 Exposure and Asthma Development: The Key Role of Oxidative Stress

Figure 4

The mechanisms of PM2.5-induced asthma. Exposure to PM2.5 can damage airway epithelial cells, cause lung inflammation and oxidative stress, and induce the release of proinflammatory cytokines (IL-6, IL-8, and TNF-α). Meanwhile, exposure to PM2.5 causes airway epithelial cells and the endoplasmic reticulum release calcium ions, which activates and phosphorylates the MAPK family, leading to increased gene transcription (NF-κB, AP-1), promoting the release of IL-6, IL-8, and TNF-α, thus activating T2 inflammatory response and inducing airway hyperresponsiveness. In addition, exposure to PM2.5 can induce autophagy through the PI3K/Akt/mTOR signaling pathway and elevate autophagy by affecting the expression of nitric oxide synthase 2 (NOS2) and the production of NO, as well as TGF-β1 expression, causing airway remodeling. SOD: superoxide dismutase; HO-1: heme oxygenase 1; AHR: airway hyperresponsiveness.