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

Figure 2

Oxidative stress in asthma airway inflammation. ROS are involved in the progression of asthma airway inflammation through three pathways. ① The increased release of ROS can result in direct oxidative damage to bronchial epithelial cells and cell shedding in asthma, which leads to the activation of epithelial cells and releases cytokines such as IL-25, IL-33, and TSLP. These cytokines promote the production of T2 cytokines from Th2 cells and ILC2s through the activation of dendritic cells (DCs), promoting type 2 inflammation. ② ROS have been implicated in the activation of transcription factors such as NF-kB and AP-1, which promotes the release of IL-6, IL-8, and TNF-α, thus activating T2 inflammatory response and resulting in impaired airway epithelium and capillary endothelial barrier function. ③ ROS can stimulate mast cells to release histamine, prostaglandin D2, and other proinflammatory mediators, as well as increase the production of mucus by airway epithelial cells, resulting in airway inflammation. ROS: reactive oxygen species; TSLP: thymic stromal lymphopoietin; NF-kB: nuclear factor kappa-B; AP-1: activator protein-1; MBP: myelin basic protein; ECP: eosinophil cationic protein; EPO: eosinophil peroxidase.