Abstract
Neutrophils constitute a critical part of innate immunity and are well known for their ability to phagocytose and kill invading microorganisms. The microbicidal processes employed by neutrophils are highly effective at killing most ingested bacteria and fungi. However, an alternative non-phagocytic antimicrobial mechanism of neutrophils has been proposed whereby microorganisms are eliminated by neutrophil extracellular traps (NETs). NETs are comprised of DNA, histones, and antimicrobial proteins extruded by neutrophils during NETosis, a cell death pathway reported to be distinct from apoptosis, phagocytosis-induced cell death, and necrosis. Although multiple laboratories have reported NETs using various stimuli in vitro, the molecular mechanisms involved in this process have yet to be definitively elucidated, and many questions regarding the formation and putative role or function of NETs in innate host defense remain unanswered. It is with these questions in mind that we provide some reflection and perspective on NETs and NETosis.
Highlights
The neutrophil lifespan is regulated by a balance of proand anti-apoptotic factors present in the environment
Molecular control of neutrophil turnover or apoptosis is mediated by several mechanisms, including extrinsic pathways induced by extracellular signals and intrinsic pathways induced by intracellular signals
Apoptosis elicited by FAS, tumor necrosis factor (TNF)-α, or TNF-related apoptosis inducing ligand (TRAIL), caused by the binding of these extracellular ligands to the cognate receptor anchored on the cell surface, is an example of extrinsic pathway apoptosis (Kennedy and DeLeo, 2009; Duffin et al, 2010)
Summary
The neutrophil lifespan is regulated by a balance of proand anti-apoptotic factors present in the environment. Neutrophil phagocytosisinduced apoptosis or phagocytosis-induced cell death (PICD) promotes the resolution of infection by disposing spent or effete neutrophils containing dead or partially digested microbes in a non-inflammatory manner (Kennedy and DeLeo, 2009).
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