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B 群链球菌 CovS/CovR 酸应答调控子是其在巨噬细胞内生存所必需的。

The CovS/CovR acid response regulator is required for intracellular survival of group B Streptococcus in macrophages.

机构信息

School of Biosciences, College of Life and Environmental Sciences, School of Biosciences, University of Birmingham, Edgbaston, Birmingham, United Kingdom.

出版信息

Infect Immun. 2012 May;80(5):1650-61. doi: 10.1128/IAI.05443-11. Epub 2012 Feb 13.

DOI:10.1128/IAI.05443-11
PMID:22331428
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3347446/
Abstract

Group B Streptococcus (GBS) is a leading cause of neonatal meningitis and septicemia. The ability of this organism to survive inside phagocytic cells is poorly understood but thought to be an important step for the establishment of disease in the host. Here, we demonstrate that GBS shows prolonged survival within J774 macrophages and that the capacity to survive is not significantly changed across a diverse range of strains representing different serotypes, multilocus sequence types (MLST), and sites of clinical isolation. Using staining for the lysosome-associated membrane protein (LAMP) and by pharmacological inhibition of phagosome acidification, we demonstrate that streptococci reside in a phagosome and that acidification of the phagosome is required for GBS to survive intracellularly. Moreover, we show that the GBS two-component system CovS/CovR, which is the major acid response regulator in this organism, is required for survival inside the phagosome.

摘要

B 群链球菌(GBS)是导致新生儿脑膜炎和败血症的主要原因。该生物体在吞噬细胞内存活的能力尚未得到充分了解,但被认为是在宿主中建立疾病的重要步骤。在这里,我们证明 GBS 在 J774 巨噬细胞内有长时间的存活能力,并且在代表不同血清型、多位点序列型(MLST)和临床分离部位的不同菌株之间,其存活能力没有明显变化。通过对溶酶体相关膜蛋白(LAMP)的染色和通过吞噬体酸化的药理学抑制,我们证明链球菌存在于吞噬体中,并且吞噬体酸化是 GBS 在细胞内存活所必需的。此外,我们还表明,GBS 的双组分系统 CovS/CovR,是该生物体中主要的酸响应调节剂,对于在吞噬体中存活是必需的。

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本文引用的文献

1
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J Neuroinflammation. 2011 Sep 26;8:123. doi: 10.1186/1742-2094-8-123.
2
Are bloodstream leukocytes Trojan Horses for the metastasis of Staphylococcus aureus?血流白细胞是金黄色葡萄球菌转移的特洛伊木马吗?
Nat Rev Microbiol. 2011 Mar;9(3):215-22. doi: 10.1038/nrmicro2508. Epub 2011 Feb 7.
3
Automated analysis of cryptococcal macrophage parasitism using GFP-tagged cryptococci.使用 GFP 标记的隐球菌进行隐球菌巨噬细胞寄生的自动分析。
PLoS One. 2010 Dec 31;5(12):e15968. doi: 10.1371/journal.pone.0015968.
4
The surface protein HvgA mediates group B streptococcus hypervirulence and meningeal tropism in neonates.表面蛋白 HvgA 介导 B 群链球菌的高致病性和对新生儿的脑膜趋向性。
J Exp Med. 2010 Oct 25;207(11):2313-22. doi: 10.1084/jem.20092594. Epub 2010 Oct 18.
5
Regulation of CovR expression in Group B Streptococcus impacts blood-brain barrier penetration.B 群链球菌 CovR 表达的调控影响血脑屏障穿透性。
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6
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Eukaryot Cell. 2010 Jun;9(6):971-80. doi: 10.1128/EC.00271-09. Epub 2010 Apr 16.
7
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J Exp Med. 2009 Aug 3;206(8):1691-9. doi: 10.1084/jem.20090691. Epub 2009 Jul 13.
8
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9
Antimicrobial mechanisms of phagocytes and bacterial evasion strategies.吞噬细胞的抗菌机制及细菌逃避策略。
Nat Rev Microbiol. 2009 May;7(5):355-66. doi: 10.1038/nrmicro2128.
10
Molecular mimicry of host sialylated glycans allows a bacterial pathogen to engage neutrophil Siglec-9 and dampen the innate immune response.宿主唾液酸化聚糖的分子模拟使一种细菌病原体能够与中性粒细胞Siglec-9结合并抑制先天免疫反应。
Blood. 2009 Apr 2;113(14):3333-6. doi: 10.1182/blood-2008-11-187302. Epub 2009 Feb 4.