期刊
CARDIOVASCULAR RESEARCH
卷 118, 期 13, 页码 2737-2753出版社
OXFORD UNIV PRESS
DOI: 10.1093/cvr/cvab329
关键词
Neutrophil; NETosis; Sterile inflammation
资金
- Deutsche Forschungsgemeinschaft [SFB914, SFB1123, SFB1009]
- Vetenskapsradet [2017-01762]
- Else-Kroner-Fresenius Stiftung [2017_A13]
- Swedish Heart-Lung Foundation [20190317]
- Leducq foundation [TNE-18CVD04]
- National Heart, Lung, and Blood Institute [1R01HL134892]
- American Heart Association [18CSA34080399]
- RRM Charitable Fund
- Simard Fund
- Cancer Research UK
- Wellcome Trust [FC0010129, FC001134]
- EMBO LTF [ALTF 113-2019]
- Ministerio de Ciencia e Innovacion [RTI2018-095497-B-I00]
- La Caixa Foundation [HR17_00527]
- European Commision [FET-OPEN 861878]
- Francis Crick institute - UK Medical Research Council
Neutrophils combat infections and injuries by releasing web-like DNA structures called neutrophil extracellular traps (NETs), which prevent pathogen dissemination or deal with larger microorganisms. However, uncontrolled release of NETs can lead to adverse effects such as vessel occlusion, tissue damage, and prolonged inflammation. This review discusses recent advances in understanding the mechanisms of NET release and functions, as well as the importance of neutrophil heterogeneity in NET formation and composition.
At the frontline of the host defence response, neutrophil antimicrobial functions have adapted to combat infections and injuries of different origins and magnitude. The release of web-like DNA structures named neutrophil extracellular traps (NETs) constitutes an important mechanism by which neutrophils prevent pathogen dissemination or deal with microorganisms of a bigger size. At the same time, nuclear and granule proteins with microbicidal activity bind to these DNA structures promoting the elimination of entrapped pathogens. However, these toxic properties may produce unwanted effects in the host, when neutrophils uncontrollably release NETs upon persistent inflammation. As a consequence, NET accumulation can produce vessel occlusion, tissue damage, and prolonged inflammation associated with the progression and exacerbation of multiple pathologic conditions. This review outlines recent advances in understanding the mechanisms of NET release and functions in sterile disease. We also discuss mechanisms of physiological regulation and the importance of neutrophil heterogeneity in NET formation and composition.
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