中性粒细胞胞外陷阱
先天免疫系统
微生物学
金黄色葡萄球菌
细胞外
肺炎链球菌
巨噬细胞
生物
吞噬作用
抗菌肽
铜绿假单胞菌
细菌
细胞生物学
免疫系统
免疫学
炎症
抗菌剂
抗生素
体外
生物化学
遗传学
作者
Andrew J. Monteith,Jeanette M. Miller,Cathy A. Maxwell,Walter Chazin,Eric P. Skaar
出处
期刊:Science Advances
[American Association for the Advancement of Science (AAAS)]
日期:2021-09-10
卷期号:7 (37)
被引量:62
标识
DOI:10.1126/sciadv.abj2101
摘要
Neutrophils and macrophages are critical to the innate immune response, but cooperative mechanisms used by these cells to combat extracellular pathogens are not well understood. This study reveals that S100A9-deficient neutrophils produce higher levels of mitochondrial superoxide in response to Staphylococcus aureus and, as a result, form neutrophil extracellular traps (suicidal NETosis). Increased suicidal NETosis does not improve neutrophil killing of S. aureus in isolation but augments macrophage killing. NET formation enhances antibacterial activity by increasing phagocytosis by macrophages and by transferring neutrophil-specific antimicrobial peptides to them. Similar results were observed in response to other phylogenetically distinct bacterial pathogens including Streptococcus pneumoniae and Pseudomonas aeruginosa, implicating this as an immune defense mechanism that broadly enhances antibacterial activity. These results demonstrate that achieving maximal bactericidal activity through NET formation requires macrophages and that accelerated and more robust suicidal NETosis makes neutrophils adept at increasing antibacterial activity, especially when A9 deficient.
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