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社区相关性耐甲氧西林金黄色葡萄球菌的免疫逃逸和毒力。

Community-associated methicillin-resistant Staphylococcus aureus immune evasion and virulence.

机构信息

Laboratory of Human Bacterial Pathogenesis, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT, 59840, USA.

出版信息

J Mol Med (Berl). 2010 Feb;88(2):109-14. doi: 10.1007/s00109-009-0573-x. Epub 2010 Jan 5.

DOI:10.1007/s00109-009-0573-x
PMID:20049412
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2852573/
Abstract

Staphylococcus aureus is a significant cause of human infections globally. Methicillin-resistant S. aureus (MRSA) emerged in the early 1960s and is now endemic in most healthcare facilities. Although healthcare-associated MRSA infections remain a major problem in most industrialized countries, those caused by community-associated MRSA (CA-MRSA) are now the most abundant cause of bacterial infections in the community in some parts of the world, such as the United States. The basis for the emergence and subsequent success of CA-MRSA is incompletely defined. However, the ability of the pathogen to cause disease in otherwise healthy individuals is likely attributed, in part, to its ability to circumvent killing by the innate immune system, which includes survival after phagocytosis by neutrophils. In this review, we discuss the role of neutrophils in host defense against S. aureus and highlight progress made toward understanding mechanisms of CA-MRSA virulence and pathogenesis.

摘要

金黄色葡萄球菌是全球范围内人类感染的重要病原体。耐甲氧西林金黄色葡萄球菌(MRSA)于 20 世纪 60 年代初出现,现已在大多数医疗机构中流行。尽管与医疗保健相关的 MRSA 感染仍然是大多数工业化国家的主要问题,但由社区相关 MRSA(CA-MRSA)引起的感染现在是世界上某些地区(如美国)社区中细菌感染的最主要原因。CA-MRSA 出现和随后成功的基础尚未完全确定。然而,病原体能够在其他健康个体中引起疾病的能力,部分归因于其逃避固有免疫系统杀伤的能力,这包括被中性粒细胞吞噬后存活。在这篇综述中,我们讨论了中性粒细胞在宿主防御金黄色葡萄球菌中的作用,并强调了在理解 CA-MRSA 毒力和发病机制方面取得的进展。

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本文引用的文献

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Reemergence of antibiotic-resistant Staphylococcus aureus in the genomics era.基因组学时代耐抗生素金黄色葡萄球菌的再度出现。
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Waves of resistance: Staphylococcus aureus in the antibiotic era.耐药浪潮:抗生素时代的金黄色葡萄球菌
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Phenol-soluble modulin alpha 3 enhances the human neutrophil lysis mediated by Panton-Valentine leukocidin.酚溶性调节素α3增强由杀白细胞素介导的人中性粒细胞溶解作用。
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Staphylococcus aureus Panton-Valentine leukocidin contributes to inflammation and muscle tissue injury.金黄色葡萄球菌杀白细胞素可导致炎症和肌肉组织损伤。
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A point mutation in the agr locus rather than expression of the Panton-Valentine leukocidin caused previously reported phenotypes in Staphylococcus aureus pneumonia and gene regulation.金黄色葡萄球菌肺炎先前报道的表型及基因调控是由agr基因座中的点突变而非杀白细胞素的表达所引起的。
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