How neutrophils die likely affects their clearance and cross-signaling to monocytes/macrophages. Apoptosis is the default mode of neutrophil death. At sites of inflammation, neutrophils undergo spontaneous apoptosis (54). In addition, neutrophil apoptosis can be induced by macrophages releasing death receptor ligands, such as TNF-α and Fas ligand (55-57). Macrophages recognize and ingest apoptotic neutrophils (54), a process known as efferocytosis. Phosphatidylserine products are externalized by neutrophils early during apoptosis and stimulate efferocytosis of neutrophils by macrophages (58, 59). In contrast, NETotic neutrophils display phosphatidylserine only after plasma membrane rupture (39). In addition, release of primary neutrophil granular...
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...dulation of the intracellular redox status (68). In addition to regulating inflammation in response to microbial constituents, NOX2 can limit inflammation in response to tissue injury. NOX2 was protective in acute acid aspiration-induced acute lung injury, limiting alveolar neutrophilic inflammation, inducing Nrf2 activation in lungs, and reducing alveolar-capillary wall leak (69, 70).
These results show that NOX2 can limit lung inflammation and injury in response to pathogens, microbial products, and direct tissue injury. Since the current understanding is that ROIs are pro-inflammatory and injurious, an anti-inflammatory effect of NOX2 – the major source of ROI generation in activated phagocytes – is paradoxical. However, through its modulation of multiple pathways involved in inflammation and injury, NOX2 can serve to resolve inflammation and limit tissue injury.
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