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本文引用的文献

1
Lipid analogs reveal features critical for hemolysis and diminish granadaene mediated Group B Streptococcus infection.脂质类似物揭示了溶血的关键特征,并减轻了格兰那定介导的 B 群链球菌感染。
Nat Commun. 2020 Mar 20;11(1):1502. doi: 10.1038/s41467-020-15282-0.
2
The Genes Reveal the Biosynthetic and Evolutionary Origins of the Group B Hemolytic Lipid, Granadaene.基因揭示了B族溶血型脂质格拉纳烯的生物合成及进化起源。
Front Microbiol. 2020 Jan 21;10:3123. doi: 10.3389/fmicb.2019.03123. eCollection 2019.
3
Streptococcus agalactiae Induces Placental Macrophages To Release Extracellular Traps Loaded with Tissue Remodeling Enzymes via an Oxidative Burst-Dependent Mechanism.无乳链球菌通过氧化爆发依赖的机制诱导胎盘巨噬细胞释放负载组织重塑酶的细胞外陷阱。
mBio. 2018 Nov 20;9(6):e02084-18. doi: 10.1128/mBio.02084-18.
4
Outer Membrane Vesicles Protect the Pathogen From Reactive Oxygen Species of the Respiratory Burst.外膜囊泡保护病原体免受呼吸爆发产生的活性氧的侵害。
Front Microbiol. 2018 Sep 7;9:1837. doi: 10.3389/fmicb.2018.01837. eCollection 2018.
5
Outer Membrane Vesicles Facilitate Trafficking of the Hydrophobic Signaling Molecule CAI-1 between Vibrio harveyi Cells.外膜囊泡促进 Harveyi 弧菌细胞间疏水信号分子 CAI-1 的运输。
J Bacteriol. 2018 Jul 10;200(15). doi: 10.1128/JB.00740-17. Print 2018 Aug 1.
6
Membrane-Derived Vesicles Promote Bacterial Virulence and Confer Protective Immunity in Murine Infection Models.膜衍生囊泡促进细菌毒力并在小鼠感染模型中赋予保护性免疫。
Front Microbiol. 2018 Feb 20;9:262. doi: 10.3389/fmicb.2018.00262. eCollection 2018.
7
Estimates of the Burden of Group B Streptococcal Disease Worldwide for Pregnant Women, Stillbirths, and Children.全球孕妇、死胎和儿童 B 群链球菌病负担估计。
Clin Infect Dis. 2017 Nov 6;65(suppl_2):S200-S219. doi: 10.1093/cid/cix664.
8
Neurodevelopmental Impairment in Children After Group B Streptococcal Disease Worldwide: Systematic Review and Meta-analyses.全球范围内 B 群链球菌疾病后儿童的神经发育障碍:系统评价和荟萃分析。
Clin Infect Dis. 2017 Nov 6;65(suppl_2):S190-S199. doi: 10.1093/cid/cix663.
9
Preterm Birth Associated With Group B Streptococcus Maternal Colonization Worldwide: Systematic Review and Meta-analyses.全球范围内与 B 族链球菌母婴定植相关的早产:系统评价和荟萃分析。
Clin Infect Dis. 2017 Nov 6;65(suppl_2):S133-S142. doi: 10.1093/cid/cix661.
10
Stillbirth With Group B Streptococcus Disease Worldwide: Systematic Review and Meta-analyses.全球范围内 B 群链球菌疾病导致的死胎:系统评价和荟萃分析。
Clin Infect Dis. 2017 Nov 6;65(suppl_2):S125-S132. doi: 10.1093/cid/cix585.

B 群链球菌溶血膜囊泡促进感染。

Hemolytic Membrane Vesicles of Group B Streptococcus Promote Infection.

机构信息

Department of Global Health, University of Washington, Seattle, Washington, USA.

Center for Global Infectious Disease Research, Seattle Children's Research Institute, Seattle, Washington, USA.

出版信息

J Infect Dis. 2021 Apr 23;223(8):1488-1496. doi: 10.1093/infdis/jiaa548.

DOI:10.1093/infdis/jiaa548
PMID:32861213
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8064051/
Abstract

BACKGROUND

Group B streptococci (GBS) are β-hemolytic, Gram-positive bacteria associated with fetal injury, preterm birth, spontaneous abortion, and neonatal infections. A key factor promoting GBS virulence is the β-hemolysin/cytolysin, a pigmented ornithine rhamnolipid (also known as granadaene) associated with the bacterial surface.

METHODS

A previous study indicated that GBS produce small structures known as membrane vesicles (MVs), which contain virulence-associated proteins. In this study, we show that GBS MVs are pigmented and hemolytic, indicating that granadaene is functionally active in MVs.

RESULTS

In addition, MVs from hyperhemolytic GBS induced greater cell death of neutrophils, T cells, and B cells compared with MVs from isogenic nonhemolytic GBS, implicating MVs as a potential mechanism for granadaene-mediated virulence. Finally, hemolytic MVs reduced oxidative killing of GBS and aggravated morbidity and mortality of neonatal mice infected with GBS.

CONCLUSIONS

These studies, taken together, reveal a novel mechanism by which GBS deploy a crucial virulence factor to promote bacterial dissemination and pathogenesis.

摘要

背景

B 群链球菌(GBS)是一种β-溶血性、革兰氏阳性细菌,与胎儿损伤、早产、自然流产和新生儿感染有关。促进 GBS 毒力的一个关键因素是β-溶血素/细胞毒素,这是一种与细菌表面相关的色素鸟氨酸鼠李糖脂(也称为格兰纳丁)。

方法

先前的一项研究表明,GBS 会产生称为膜泡(MVs)的小结构,其中包含与毒力相关的蛋白质。在这项研究中,我们表明 GBS MVs 是色素沉着和溶血的,表明格兰纳丁在 MVs 中具有功能活性。

结果

此外,与同源非溶血 GBS 的 MVs 相比,高溶血 GBS 的 MVs 诱导更多的中性粒细胞、T 细胞和 B 细胞死亡,这表明 MVs 是格兰纳丁介导的毒力的潜在机制。最后,溶血 MVs 降低了 GBS 的氧化杀伤作用,并加重了感染 GBS 的新生小鼠的发病率和死亡率。

结论

这些研究共同揭示了 GBS 部署关键毒力因子以促进细菌传播和发病机制的新机制。