Figure 2.

(A) Active NADPH oxidase complexes promote ROS production. The activated NADPH oxidase complex uses fad to transfer electrons (e^-) to oxygen to form $O_2^{-}$ from phagocytes. $O_2^{-}$ is produced by the activation of NADPH oxidase. $O_2^{-}$. $O_2^{-}$ from phagocytes. $O_2^{-}$ is produced by the activation of NADPH oxidase. $O_2^{-}$ produced by NADPH oxidase can react with protons to form H₂O₂, which in turn produces HOCl under the action of MPO. $O_2^{-}$ from phagocytes. $O_2^{-}$ is produced by the activation of NADPH oxidase. $O_2^{-}$ can react with H₂O₂ in the presence of Fe²⁺ or Cu²⁺ to form OH- or ROS. (B) The role of neutrophil activation in host defense and the inflammatory response. As shown on the left side, the initiation of proinflammatory cytokines or microbial molecules under physiological conditions is an immune-monitoring mechanism that ultimately enhances the antibacterial activity of neutrophils. However, as shown on the right side, excessive activation of neutrophil NADPH oxidase leads to excessive production of ROS, causing tissue damage and an excessive inflammatory response. Mediated by various proinflammatory mediators, receptor signals on the vascular endothelial surface are involved in neutrophil rolling, adhesion and endothelial barrier crossing. Phagocytosis of neutrophils leads to the activation of a series of processes, leading to the release of antimicrobial peptides, proteases, MPO and $O_2^{-}$ from phagocytes. $O_2^{-}$ is produced by the activation of NADPH oxidase. $O_2^{-}$, which is produced by the activation of NADPH oxidase, from phagocytes.