Neutrophil apoptosis and the resolution of infection

被引:275
作者
Kennedy, Adam D. [1 ]
Deleo, Frank R. [1 ]
机构
[1] NIAID, Lab Human Bacterial Pathogenesis, Rocky Mt Labs, NIH, Hamilton, MT 59840 USA
基金
美国国家卫生研究院;
关键词
Neutrophil; Cell death; Apoptosis; Phagocytosis; Pyroptosis; Autophagy; Macrophage; Inflammation; Pathogen; Innate immunity; TUMOR-NECROSIS-FACTOR; PROGRAMMED CELL-DEATH; HUMAN POLYMORPHONUCLEAR LEUKOCYTES; RESISTANT STAPHYLOCOCCUS-AUREUS; TUBERCULOSIS-INDUCED APOPTOSIS; TOLL-LIKE RECEPTOR; HUMAN BONE-MARROW; 11-BETA-HYDROXYSTEROID DEHYDROGENASE TYPE-1; VIRULENT MYCOBACTERIUM-TUBERCULOSIS; MANNHEIMIA-HAEMOLYTICA LEUKOTOXIN;
D O I
10.1007/s12026-008-8049-6
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Polymorphonuclear leukocytes (PMNs) are the most abundant white cell in humans and an essential component of the innate immune system. PMNs are typically the first type of leukocyte recruited to sites of infection or areas of inflammation. Ingestion of microorganisms triggers production of reactive oxygen species and fusion of cytoplasmic granules with forming phagosomes, leading to effective killing of ingested microbes. Phagocytosis of bacteria typically accelerates neutrophil apoptosis, which ultimately promotes the resolution of infection. However, some bacterial pathogens alter PMN apoptosis to survive and thereby cause disease. Herein, we review PMN apoptosis and the ability of microorganisms to alter this important process.
引用
收藏
页码:25 / 61
页数:37
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