Matters of life and death. How neutrophils die or survive along NET release and is “NETosis” = necroptosis?

Neutrophil extracellular trap (NET) formation is a hallmark of many disorders that involve neutrophil recruitment, tissue damage, and inflammation. As NET formation is often associated with neutrophil death, the term “NETosis” has become popular. Upon discovery that neutrophils may survive NET relea...

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Published inCellular and molecular life sciences : CMLS Vol. 73; no. 11-12; pp. 2211 - 2219
Main Authors Desai, Jyaysi, Mulay, Shrikant R., Nakazawa, Daigo, Anders, Hans-Joachim
Format Journal Article
LanguageEnglish
Published Cham Springer International Publishing 01.06.2016
Springer Nature B.V
Subjects
Apoptosis
Apoptosis - immunology
Biochemistry
Biomedical and Life Sciences
Biomedicine
Bone marrow
Cell Biology
Chromatin
Extracellular Traps - immunology
Humans
Inflammation - immunology
Inflammation - pathology
Life Sciences
Mortality
Multi-Author Review
Necrosis - immunology
Neutrophils - immunology
Protein Kinases - metabolism
Receptor-Interacting Protein Serine-Threonine Kinases - metabolism
Signal transduction
Signal Transduction - immunology
Infection
Histones
Regulated necrosis
Host defense
Sterile inflammation
Gout
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Summary:Neutrophil extracellular trap (NET) formation is a hallmark of many disorders that involve neutrophil recruitment, tissue damage, and inflammation. As NET formation is often associated with neutrophil death, the term “NETosis” has become popular. Upon discovery that neutrophils may survive NET release, apparent misnomers, such as “vital NETosis,” have been proposed. Meanwhile, it has become obvious that certain stimuli can trigger neutrophil necroptosis, a process associated with NET-like chromatin release. Here, we discuss the relationship between NET release and neutrophil death in view highlighting that many assays used in the field do not properly distinguish between the two. An updated nomenclature is needed replacing the term “NETosis” to meet the growing variety of settings leading to chromatin release with and without neutrophil death. Dissecting which triggers of NET release involve which signaling pathway will help to define drugable molecular targets that inhibit NET release and/or neutrophil necrosis in specific disorders.
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ISSN:1420-682X
1420-9071
DOI:10.1007/s00018-016-2195-0