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宿主与金黄色葡萄球菌蛋白酶系统的相互作用调节其毒力和致病性。

Interaction of host and Staphylococcus aureus protease-system regulates virulence and pathogenicity.

机构信息

Molecular Bioprospection Department, CSIR-Central Institute of Medicinal and Aromatic Plants, P.O. CIMAP, Lucknow, 226015, India.

School of Life Science, Jawaharlal Nehru University, New Delhi, 110067, India.

出版信息

Med Microbiol Immunol. 2019 Oct;208(5):585-607. doi: 10.1007/s00430-018-0573-y. Epub 2018 Nov 27.

DOI:10.1007/s00430-018-0573-y
PMID:30483863
Abstract

Staphylococcus aureus causes various health care- and community-associated infections as well as certain chronic TH2 driven inflammatory diseases. It is a potent pathogen with serious virulence and associated high morbidity. Severe pathogenicity is accredited to the S. aureus secreted virulence factors such as proteases and host protease modulators. These virulence factors promote adhesion and invasion of bacteria through damage of tight junction barrier and keratinocytes. They inhibit activation and transmigration of various immune cells such as neutrophils (and neutrophil proteases) to evade opsono-phagocytosis and intracellular bacterial killing. Additionally, they protect the bacteria from extracellular killing by disrupting integrity of extracellular matrix. Platelet activation and agglutination is also impaired by these factors. They also block the classical as well as alternative pathways of complement activation and assist in spread of infection through blood and tissue. As these factors are exquisite factors of S. aureus mediated disease development, we have focused on review of diversification of various protease-system associated virulence factors, their structural building, diverse role in disease development and available therapeutic counter measures. This review summarises the role of protease-associated virulence factors during invasion and progression of disease.

摘要

金黄色葡萄球菌可引起各种医疗保健相关和社区相关感染,以及某些慢性 TH2 驱动的炎症性疾病。它是一种具有严重毒力和相关高发病率的强效病原体。严重的致病性归因于金黄色葡萄球菌分泌的毒力因子,如蛋白酶和宿主蛋白酶调节剂。这些毒力因子通过破坏紧密连接屏障和角蛋白细胞促进细菌的黏附和侵袭。它们抑制各种免疫细胞(如中性粒细胞(和中性粒细胞蛋白酶)的激活和迁移,以逃避吞噬作用和细胞内细菌杀伤。此外,它们通过破坏细胞外基质的完整性来保护细菌免受细胞外杀伤。血小板的激活和聚集也被这些因素所破坏。它们还阻断经典和替代途径的补体激活,并通过血液和组织协助感染的传播。由于这些因子是金黄色葡萄球菌介导的疾病发展的精细因子,我们专注于综述各种与蛋白酶系统相关的毒力因子的多样化、它们的结构构建、在疾病发展中的多种作用以及可用的治疗对策。这篇综述总结了蛋白酶相关毒力因子在疾病侵袭和进展过程中的作用。

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