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金黄色葡萄球菌成孔毒素:病原体与宿主复杂性的交汇点。

Staphylococcus aureus pore-forming toxins: The interface of pathogen and host complexity.

机构信息

Department of Pediatrics, The University of Chicago, Chicago, IL 60637, United States; Department of Microbiology, The University of Chicago, Chicago, IL 60637, United States.

Department of Pediatrics, Washington University, St. Louis, MO 63110, United States.

出版信息

Semin Cell Dev Biol. 2017 Dec;72:101-116. doi: 10.1016/j.semcdb.2017.04.003. Epub 2017 Apr 23.

Abstract

Staphylococcus aureus is a prominent human pathogen capable of infecting a variety of host species and tissue sites. This versatility stems from the pathogen's ability to secrete diverse host-damaging virulence factors. Among these factors, the S. aureus pore-forming toxins (PFTs) α-toxin and the bicomponent leukocidins, have garnered much attention for their ability to lyse cells at low concentrations and modulate disease severity. Although many of these toxins were discovered nearly a century ago, their host cell specificities have only been elucidated over the past five to six years, starting with the discovery of the eukaryotic receptor for α-toxin and rapidly followed by identification of the leukocidin receptors. The identification of these receptors has revealed the species- and cell type-specificity of toxin binding, and provided insight into non-lytic effects of PFT intoxication that contribute to disease pathogenesis.

摘要

金黄色葡萄球菌是一种重要的人类病原体,能够感染多种宿主物种和组织部位。这种多功能性源于病原体分泌多种宿主损伤毒力因子的能力。在这些因子中,金黄色葡萄球菌形成孔的毒素 (PFT)α-毒素和双组分白细胞毒素,因其能够在低浓度下裂解细胞并调节疾病严重程度而受到广泛关注。尽管这些毒素中的许多在近一个世纪前就被发现了,但直到过去五到六年,随着α-毒素的真核受体的发现以及白细胞毒素受体的快速鉴定,它们的宿主细胞特异性才被阐明。这些受体的鉴定揭示了毒素结合的物种和细胞类型特异性,并深入了解了 PFT 中毒的非裂解作用如何导致疾病发病机制。

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1
Humanized Mice Exhibit Increased Susceptibility to Staphylococcus aureus Pneumonia.
J Infect Dis. 2017 May 1;215(9):1386-1395. doi: 10.1093/infdis/jiw425.
3
Necroptosis Promotes Staphylococcus aureus Clearance by Inhibiting Excessive Inflammatory Signaling.
Cell Rep. 2016 Aug 23;16(8):2219-2230. doi: 10.1016/j.celrep.2016.07.039. Epub 2016 Aug 11.
4
Staphylococcus aureus α-toxin-mediated cation entry depolarizes membrane potential and activates p38 MAP kinase in airway epithelial cells.
Am J Physiol Lung Cell Mol Physiol. 2016 Sep 1;311(3):L676-85. doi: 10.1152/ajplung.00090.2016. Epub 2016 Aug 5.
6
ADAM10-Dependent Signaling Through Notch1 and Notch4 Controls Development of Organ-Specific Vascular Beds.
Circ Res. 2016 Aug 5;119(4):519-31. doi: 10.1161/CIRCRESAHA.115.307738. Epub 2016 Jun 27.
8
Identification and treatment of the Staphylococcus aureus reservoir in vivo.
J Exp Med. 2016 Jun 27;213(7):1141-51. doi: 10.1084/jem.20160334. Epub 2016 Jun 20.
9
Dissecting the role of ADAM10 as a mediator of Staphylococcus aureus α-toxin action.
Biochem J. 2016 Jul 1;473(13):1929-40. doi: 10.1042/BCJ20160062. Epub 2016 May 4.
10
The intersection of cell death and inflammasome activation.
Cell Mol Life Sci. 2016 Jun;73(11-12):2349-67. doi: 10.1007/s00018-016-2205-2. Epub 2016 Apr 11.

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