Cellular Mechanisms of NETosis

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  • Hawa Racine Thiam
    Cell and Developmental Biology Center, National Heart, Lung, and Blood Institute (NHLBI), National Institutes of Health, Bethesda, Maryland 20892, USA;,
  • Siu Ling Wong
    Lee Kong Chian School of Medicine, Nanyang Technological University, Singapore 308232
  • Denisa D. Wagner
    Program in Cellular and Molecular Medicine, Boston Children's Hospital, Boston, Massachusetts 02115, USA
  • Clare M. Waterman
    Cell and Developmental Biology Center, National Heart, Lung, and Blood Institute (NHLBI), National Institutes of Health, Bethesda, Maryland 20892, USA;,

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<jats:p>Neutrophils are critical to innate immunity, including host defense against bacterial and fungal infections. They achieve their host defense role by phagocytosing pathogens, secreting their granules full of cytotoxic enzymes, or expelling neutrophil extracellular traps (NETs) during the process of NETosis. NETs are weblike DNA structures decorated with histones and antimicrobial proteins released by activated neutrophils. Initially described as a means for neutrophils to neutralize pathogens, NET release also occurs in sterile inflammation, promotes thrombosis, and can mediate tissue damage. To effectively manipulate this double-edged sword to fight a particular disease, researchers must work toward understanding the mechanisms driving NETosis. Such understanding would allow the generation of new drugs to promote or prevent NETosis as needed. While knowledge regarding the (patho)physiological roles of NETosis is accumulating, little is known about the cellular and biophysical bases of this process. In this review, we describe and discuss our current knowledge of the molecular, cellular, and biophysical mechanisms mediating NET release as well as open questions in the field.</jats:p>

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