The phagocyte NADPH oxidase (NOX2) is a crucial enzyme in antimicrobial host defense and in regulating inflammation. Patients with chronic granulomatous disease (CGD), an inherited disorder of NOX2 in which phagocytes are defective in generation of reactive oxidant intermediates (ROIs), suffer from life-threatening bacterial and fungal infections (8). Among CGD patients, the degree of impairment of NOX2 in neutrophils correlates with mortality (9). NOX2 is rapidly activated by conditions that, in nature, are associated with infectious threat, such as ligation of specific pathogen recognition receptors (PRRs) by microbial products (e.g., formylated peptides and fungal cell wall beta-glucans), opsonized particles, and integrin-dependent adhesion (6, 10, 11). Activation of NOX2 requires translocation of cytoplasmic subunits p47phox, p67phox...
... middle of paper ...
...as reduced, but not eliminated, in NOX2-deficient mice (49). In this model, NOX2 may trigger NETosis directly or through stimulation of IFN-γ, which was shown to augment NETosis. In murine pulmonary aspergillosis, NOX2 was required for NET generation, which is posited to limit hyphal parenchymal invasion (41).
NOX2 can therefore target pathogens through a multi-step process: (i) direct killing from NOX2-MPO-generated ROIs; (ii) activation of primary granular proteases that target phagocytosed pathogens; and (iii) generation of NETs that target extracellular pathogens. Depending on the stimulus, NETs can also be induced by NOX2-independent pathways (50-52). Douda et al. (53) showed that NETosis can be activated by mitochondrial ROIs independently of NOX2, through a pathway dependent on calcium-induced activation of SK3 (small conductance potassium channels) and Akt.
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