Staphylococcus aureus: new evidence for intracellular persistence

金黄色葡萄球菌 细胞内 生物 持久性(不连续性) 细胞外 微生物学 细胞内寄生虫 抗生素 寄主(生物学) 葡萄球菌感染 免疫学 细菌 细胞生物学 遗传学 岩土工程 工程类
作者
Christian Garzoni,William L. Kelley
出处
期刊:Trends in Microbiology [Elsevier BV]
卷期号:17 (2): 59-65 被引量:441
标识
DOI:10.1016/j.tim.2008.11.005
摘要

Many reports have documented that Staphylococcus aureus can invade host cells and persist intracellularly for various periods of time in cell culture models. However, it is not clear whether intracellular persistence of S. aureus also occurs in the course of infections in whole organisms. This is a subject of intense debate and is difficult to assess experimentally. Intracellular persistence would provide S. aureus with an ideal strategy to escape from professional phagocytes and extracellular antibiotics and would promote recrudescent infection. Here, we present a brief overview of the mounting evidence that S. aureus has the potential to internalize and survive within host cells. Many reports have documented that Staphylococcus aureus can invade host cells and persist intracellularly for various periods of time in cell culture models. However, it is not clear whether intracellular persistence of S. aureus also occurs in the course of infections in whole organisms. This is a subject of intense debate and is difficult to assess experimentally. Intracellular persistence would provide S. aureus with an ideal strategy to escape from professional phagocytes and extracellular antibiotics and would promote recrudescent infection. Here, we present a brief overview of the mounting evidence that S. aureus has the potential to internalize and survive within host cells. a potent exotoxin of S. aureus (encoded by the hla gene) that damages host-cell membrane. a highly regulated and complex form of controlled cell death, which most often occurs without an inflammatory response. requiring a specific growth substance. Especially used to describe physiological consequences of mutation. molecular chaperones of the heat-shock protein 100 family involved in protein refolding and degradation, some of which are regulatory components of the Clp proteolytic complex. a surface protein of S. aureus, which binds fibrinogen and is classed as a microbial surface component recognizing adhesive-matrix molecules (MSCRAMMs). Although ClfA is structurally related to clumping factor B, they have different properties. fungal toxin that binds actin and disrupts filaments and actin polymerization. a term used to describe filamentous or fibrous actin (as opposed to globular actin, the constituent subunit). a soluble plasma glycoprotein that is a precursor of fibrin. a constituent glycoprotein of the extracellular matrix of most body tissues, as well as a soluble form in body fluids. S. aureus fibronectin-binding proteins A and B (FnBPs) are structurally related MSCRAMMs covalently anchored to the peptidoglycan. a family of α/β heterodimeric integral membrane proteins mediating adhesion and transmembrane signalling. factors, most often proteinaceous, mediating microbial invasion into host cells. inflammation of mammary gland or udder caused by infection. ratio of the number of microbes (bacteria or viruses) to host cells. cell death that occurs because of inadequate blood supply and often results in a substantial inflammatory response. bone infection. inflammation of the nose and paranasal sinuses. the abbreviation SCCmec refers to a classification nomenclature of Staphylococcal cassette chromosomal element (probably mobile) encoding the mecA gene encoding penicillin-binding protein 2a. staphylococcal protein A encoded by spa.
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