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Editorial
. 2020 Apr 3;55(4):2000305.
doi: 10.1183/13993003.00305-2020. Print 2020 Apr.

NETs: a new biomarker of traffic-related air pollution exposure: are they ready to catch fish?

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Editorial

NETs: a new biomarker of traffic-related air pollution exposure: are they ready to catch fish?

Howard M Kipen et al. Eur Respir J. .
No abstract available

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Conflict of interest statement

Conflict of interest: H.M. Kipen has nothing to disclose. Conflict of interest: D.L. Laskin has nothing to disclose.

Figures

FIGURE 1
FIGURE 1
Polymorphonuclear leukocyte (PMN) neutrophil NETosis. Left: Suicidal NETosis. A key initiating step in suicidal NETosis is activation of NADPH oxidase and reactive oxygen species (ROS) production. ROS cause activation of peptidyl arginine deiminase 4 (PAD4) and rupture of cytoplasmic granules, releasing myeloperoxidase (MPO) and neutrophil elastase (NE). MPO and NE translocate to the nucleus and together with PAD4 cause chromatin decondensation. This leads to rupture of the nuclear membrane and release of chromatin into the cytoplasm where it is decorated with granular and cytoplasmic proteins. Neutrophil extracellular traps (NETs) are released following plasma membrane rupture. This process typically requires several hours and culminates in PMN lysis and death. Right: Vital NETosis. Following activation of Toll-like receptors (TLRs) by pathogens and/or platelets, PAD4 is activated and NE and MPO released causing chromatin decondensation. Chromatin is decorated and released into the cytoplasm within vesicles formed by blebbing of the nuclear membrane, a process which ultimately leads to nuclear membrane rupture. Vesicles containing NETs are released from PMN via exocytosis leaving the plasma membrane intact and the anuclear PMN capable of phagocytosis and chemotaxis. This process occurs within minutes of initiation.

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