The Effect Of Nox2 On Macrophages And Neutrophils As Critical Modulators Of Inflammation

The Effect Of Nox2 On Macrophages And Neutrophils As Critical Modulators Of Inflammation

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In addition to host defense, there is a growing body of evidence supporting NOX2 in macrophages and neutrophils as critical modulators of inflammation. Neutrophils are rapidly recruited to sites of infection and trauma by activation of specific G-protein coupled receptors that are ligated by formylated peptides produced by bacteria and by host-derived chemoattractants, such as leukotriene B4, C5a, and chemokines (e.g., MIP-2 and interleukin-8). Activation of specific PRRs generally leads to NF-kB activation and production of pro-inflammatory cytokines. Termination of neutrophilic inflammation, essential to limit excessive tissue damage, is an active process regulated by several anti-inflammatory pathways that include neutrophil apoptosis and clearance and suppression of cytokine/chemokine responses. While the immediate effect of NOX2 activation – generation of ROIs and activation of proteases – is expected to increase tissue injury, NOX2 activation can also limit inflammation and injury.
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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