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The Vi capsular polysaccharide prevents complement receptor 3-mediated clearance of Salmonella enterica serotype Typhi.荚膜多糖 Vi 阻止了沙门氏菌属肠道亚种 Typhi 经补体受体 3 介导的清除。
Infect Immun. 2011 Feb;79(2):830-7. doi: 10.1128/IAI.00961-10. Epub 2010 Nov 22.
2
Loss of very-long O-antigen chains optimizes capsule-mediated immune evasion by Salmonella enterica serovar Typhi.伤寒沙门氏菌血清型 Typhi 丧失超长 O-抗原链可优化荚膜介导的免疫逃避。
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3
Rifampin mediated decapsulation and enhanced bacterial clearance: a new mechanism of rifamycins.利福平介导的去包膜作用及增强细菌清除作用:利福霉素的一种新机制。
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The Salmonella enterica serotype Typhi Vi capsular antigen is expressed after the bacterium enters the ileal mucosa.沙门氏菌血清型 Typhi Vi 荚膜抗原在细菌进入回肠黏膜后表达。
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Propionylation of Fis K32 in serovar Typhi: a key modification affecting pathogenicity.伤寒杆菌中Fis K32的丙酰化:影响致病性的关键修饰
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The Vi capsular polysaccharide enables Salmonella enterica serovar typhi to evade microbe-guided neutrophil chemotaxis.Vi 荚膜多糖使伤寒沙门氏菌能够逃避微生物引导的中性粒细胞趋化作用。
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The Lack of Natural IgM Increases Susceptibility and Impairs Anti-Vi Polysaccharide IgG Responses in a Mouse Model of Typhoid.天然 IgM 的缺乏会增加伤寒小鼠模型的易感性并损害抗 Vi 多糖 IgG 应答。
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The Vi Capsular Polysaccharide of Salmonella Typhi Promotes Macrophage Phagocytosis by Binding the Human C-Type Lectin DC-SIGN.伤寒沙门氏菌 Vi 荚膜多糖通过结合人 C 型凝集素 DC-SIGN 促进巨噬细胞吞噬作用。
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OxyR positively and directly regulates Vi polysaccharide capsular antigen in Salmonella enterica serovar Typhi.OxyR 正向且直接调控伤寒沙门氏菌血清型 Vi 多糖荚膜抗原。
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引用本文的文献

1
Rifampin mediated decapsulation and enhanced bacterial clearance: a new mechanism of rifamycins.利福平介导的去包膜作用及增强细菌清除作用:利福霉素的一种新机制。
EBioMedicine. 2025 Jun 3;117:105787. doi: 10.1016/j.ebiom.2025.105787.
2
Genetic engineering of E. coli K-12 for heterologous carbohydrate antigen production.用于异源碳水化合物抗原生产的大肠杆菌K-12基因工程。
Microb Cell Fact. 2025 May 28;24(1):126. doi: 10.1186/s12934-025-02749-2.
3
Evasion of serum antibodies and complement by Salmonella Typhi and Paratyphi A.伤寒沙门氏菌和甲型副伤寒沙门氏菌对血清抗体和补体的逃避
PLoS Pathog. 2025 May 2;21(5):e1012917. doi: 10.1371/journal.ppat.1012917. eCollection 2025 May.
4
Virulence factors of Salmonella Typhi: interplay between the bacteria and host macrophages.伤寒沙门氏菌的毒力因子:细菌与宿主巨噬细胞之间的相互作用
Arch Microbiol. 2025 Mar 17;207(4):89. doi: 10.1007/s00203-025-04297-0.
5
Single missense mutations in Vi capsule synthesis genes confer hypervirulence to Salmonella Typhi.单个错义突变在 Vi 荚膜合成基因赋予伤寒沙门氏菌高毒力。
Nat Commun. 2024 Jun 19;15(1):5258. doi: 10.1038/s41467-024-49590-6.
6
Transcriptional profiling links unique human macrophage phenotypes to the growth of intracellular Salmonella enterica serovar Typhi.转录谱分析将独特的人类巨噬细胞表型与细胞内伤寒沙门氏菌 Typhi 的生长联系起来。
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High-throughput fitness experiments reveal specific vulnerabilities of human-adapted Salmonella during stress and infection.高通量适应性实验揭示了适应人类的沙门氏菌在应激和感染过程中的特定脆弱性。
Nat Genet. 2024 Jun;56(6):1288-1299. doi: 10.1038/s41588-024-01779-7. Epub 2024 Jun 3.
8
Determinants of bacterial survival and proliferation in blood.血液中细菌存活和增殖的决定因素。
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9
Molecular insights into capsular polysaccharide secretion.对荚膜多糖分泌的分子见解。
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10
Nuclear factor kappa B-dependent persistence of Typhi and Paratyphi in human macrophages.核因子 kappa B 依赖性伤寒和副伤寒在人巨噬细胞中的持续存在。
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本文引用的文献

1
The blessings and curses of intestinal inflammation.肠道炎症的福与祸。
Cell Host Microbe. 2010 Jul 22;8(1):36-43. doi: 10.1016/j.chom.2010.06.003.
2
Enteric fever in a UK regional infectious diseases unit: a 10 year retrospective review.英国地区传染病科肠热病:十年回顾性研究。
J Infect. 2010 Feb;60(2):91-8. doi: 10.1016/j.jinf.2009.11.009. Epub 2009 Dec 3.
3
Clinical pathogenesis of typhoid fever.伤寒热的临床发病机制。
J Infect Dev Ctries. 2008 Aug 30;2(4):260-6. doi: 10.3855/jidc.219.
4
The capsule-encoding viaB locus reduces intestinal inflammation by a Salmonella pathogenicity island 1-independent mechanism.通过B位点的荚膜编码通过一种不依赖沙门氏菌致病岛1的机制减轻肠道炎症。
Infect Immun. 2009 Jul;77(7):2932-42. doi: 10.1128/IAI.00172-09. Epub 2009 May 18.
5
From bench to bedside: stealth of enteroinvasive pathogens.从 bench 到 bedside:肠道侵袭性病原体的隐秘性 (注:“bench”和“bedside”在这里可能是比喻研究阶段,“bench”指实验室研究,“bedside”指临床应用,可根据具体语境理解更准确含义 )
Nat Rev Microbiol. 2008 Dec;6(12):883-92. doi: 10.1038/nrmicro2012. Epub 2008 Oct 28.
6
The Salmonella enterica serotype Typhi regulator TviA reduces interleukin-8 production in intestinal epithelial cells by repressing flagellin secretion.肠炎沙门氏菌伤寒血清型调节因子TviA通过抑制鞭毛蛋白分泌来减少肠道上皮细胞中白细胞介素-8的产生。
Cell Microbiol. 2008 Jan;10(1):247-61. doi: 10.1111/j.1462-5822.2007.01037.x.
7
Systemic translocation of Salmonella enterica serovar Dublin in cattle occurs predominantly via efferent lymphatics in a cell-free niche and requires type III secretion system 1 (T3SS-1) but not T3SS-2.肠炎沙门氏菌都柏林血清型在牛体内的全身转移主要通过无细胞微环境中的输出淋巴管发生,并且需要1型三型分泌系统(T3SS-1),而不需要T3SS-2。
Infect Immun. 2007 Nov;75(11):5191-9. doi: 10.1128/IAI.00784-07. Epub 2007 Aug 27.
8
The capsule encoding the viaB locus reduces interleukin-17 expression and mucosal innate responses in the bovine intestinal mucosa during infection with Salmonella enterica serotype Typhi.在感染伤寒沙门氏菌血清型伤寒期间,编码viaB位点的荚膜会降低牛肠道黏膜中白细胞介素-17的表达和黏膜固有免疫反应。
Infect Immun. 2007 Sep;75(9):4342-50. doi: 10.1128/IAI.01571-06. Epub 2007 Jun 25.
9
Mice lacking components of adaptive immunity show increased Brucella abortus virB mutant colonization.缺乏适应性免疫成分的小鼠显示出布鲁氏菌流产virB突变体定植增加。
Infect Immun. 2007 Jun;75(6):2965-73. doi: 10.1128/IAI.01896-06. Epub 2007 Apr 9.
10
Capsule-mediated immune evasion: a new hypothesis explaining aspects of typhoid fever pathogenesis.荚膜介导的免疫逃避:一种解释伤寒热发病机制某些方面的新假说。
Infect Immun. 2006 Jan;74(1):19-27. doi: 10.1128/IAI.74.1.19-27.2006.

荚膜多糖 Vi 阻止了沙门氏菌属肠道亚种 Typhi 经补体受体 3 介导的清除。

The Vi capsular polysaccharide prevents complement receptor 3-mediated clearance of Salmonella enterica serotype Typhi.

机构信息

Department of Medical Microbiology and Immunology, School of Medicine, University of California at Davis, One Shields Ave., Davis, CA 95616-8645, USA.

出版信息

Infect Immun. 2011 Feb;79(2):830-7. doi: 10.1128/IAI.00961-10. Epub 2010 Nov 22.

DOI:10.1128/IAI.00961-10
PMID:21098104
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3028862/
Abstract

Capsular polysaccharides are important virulence factors of invasive bacterial pathogens. Here we studied the role of the virulence (Vi) capsular polysaccharide of Salmonella enterica serotype Typhi (S. Typhi) in preventing innate immune recognition by complement. Comparison of capsulated S. Typhi with a noncapsulated mutant (ΔtviBCDE vexABCDE mutant) revealed that the Vi capsule interfered with complement component 3 (C3) deposition. Decreased complement fixation resulted in reduced bacterial binding to complement receptor 3 (CR3) on the surface of murine macrophages in vitro and decreased CR3-dependent clearance of Vi capsulated S. Typhi from the livers and spleens of mice. Opsonization of bacteria with immune serum prior to intraperitoneal infection increased clearance of capsulated S. Typhi from the liver. Our data suggest that the Vi capsule prevents CR3-dependent clearance, which can be overcome in part by a specific antibody response.

摘要

荚膜多糖是侵袭性细菌病原体的重要毒力因子。在这里,我们研究了肠伤寒沙门氏菌血清型 Typhi (S. Typhi) 的毒力(Vi)荚膜多糖在防止补体固有免疫识别中的作用。比较有荚膜的 S. Typhi 与无荚膜突变体(ΔtviBCDE vexABCDE 突变体)表明,Vi 荚膜干扰补体成分 3 (C3) 的沉积。补体固定减少导致细菌与鼠巨噬细胞表面补体受体 3 (CR3) 的结合减少,从而降低 Vi 荚膜包裹的 S. Typhi 从肝脏和脾脏中清除的 CR3 依赖性。在腹腔感染前用免疫血清对细菌进行调理,可增加肝脏中荚膜包裹的 S. Typhi 的清除率。我们的数据表明,Vi 荚膜阻止了 CR3 依赖性的清除,而这种清除可以部分被特异性抗体反应所克服。