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The inside story of Shigella invasion of intestinal epithelial cells.志贺氏菌侵袭肠上皮细胞的内幕。
Cold Spring Harb Perspect Med. 2013 Oct 1;3(10):a016717. doi: 10.1101/cshperspect.a016717.
2
Shigella spp. and enteroinvasive Escherichia coli pathogenicity factors.志贺氏菌属和肠侵袭性大肠杆菌的致病因素。
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3
Molecular and cellular mechanisms of invasion of the intestinal barrier by enteric pathogens. The paradigm of Shigella.肠道病原体侵袭肠道屏障的分子和细胞机制。志贺氏菌范例。
Folia Microbiol (Praha). 1998;43(3):239-46. doi: 10.1007/BF02818608.
4
[Modern views on the pathogenesis of dysentery: the role of invasion and the toxic action of Shigella].[关于痢疾发病机制的现代观点:志贺菌侵袭作用和毒性作用的角色]
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Mapping of Shigella flexneri's tissue distribution and type III secretion apparatus activity during infection of the large intestine of guinea pigs.在感染豚鼠大肠过程中对福氏志贺菌组织分布和 III 型分泌系统活性的定位研究。
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Shigella infection of intestinal epithelium and circumvention of the host innate defense system.志贺氏菌感染肠道上皮细胞和规避宿主先天防御系统。
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[Shigella: from the rupture to the invasion and to the destruction of the colonic epithelium].[志贺氏菌:从结肠上皮细胞破裂到入侵再到破坏]
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Shigella interaction with intestinal epithelial cells determines the innate immune response in shigellosis.志贺氏菌与肠道上皮细胞的相互作用决定了志贺氏菌病中的固有免疫反应。
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Can Nature Overcome Invasive Gastrointestinal Infections?自然能够战胜侵袭性胃肠道感染吗?
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Differential invasiveness & expression of antimicrobial peptides in serotypes.血清型中抗菌肽的侵袭性和表达的差异
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Functional assays to evaluate antibody-mediated responses against : a review.评估针对:的抗体介导反应的功能检测。一种综述。
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Mucosal Immune Profiles Associated with Diarrheal Disease Severity in - and Enteropathogenic Escherichia coli-Infected Children Enrolled in the Global Enteric Multicenter Study.黏膜免疫特征与全球肠道多中心研究中感染肠致病性大肠杆菌的腹泻病严重程度的关系。
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The type 3 secretion effector IpgD promotes S. flexneri dissemination.III 型分泌效应因子 IpgD 促进福氏志贺菌的传播。
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An in vivo acute toxicity and anti-shigellosis effect of designed formulation on rat.设计制剂对大鼠的体内急性毒性及抗志贺氏菌病作用
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本文引用的文献

1
Actin-based confinement of calcium responses during Shigella invasion.肌动蛋白限制志贺氏菌入侵过程中的钙反应。
Nat Commun. 2013;4:1567. doi: 10.1038/ncomms2561.
2
Functional insights into the Shigella type III needle tip IpaD in secretion control and cell contact.在分泌控制和细胞接触中探究志贺氏菌 III 型针尖端 IpaD 的功能见解。
Mol Microbiol. 2013 Apr;88(2):268-82. doi: 10.1111/mmi.12185. Epub 2013 Mar 11.
3
Bruton's tyrosine kinase regulates Shigella flexneri dissemination in HT-29 intestinal cells.布鲁顿酪氨酸激酶调节福氏志贺菌在 HT-29 肠细胞中的传播。
Infect Immun. 2013 Feb;81(2):598-607. doi: 10.1128/IAI.00853-12. Epub 2012 Dec 10.
4
Shigella flexneri T3SS effector IpaH4.5 modulates the host inflammatory response via interaction with NF-κB p65 protein.志贺氏杆菌 T3SS 效应因子 IpaH4.5 通过与 NF-κB p65 蛋白相互作用来调节宿主炎症反应。
Cell Microbiol. 2013 Mar;15(3):474-85. doi: 10.1111/cmi.12052. Epub 2012 Nov 13.
5
Antivirulence genes: insights into pathogen evolution through gene loss.抗病毒基因:通过基因缺失了解病原体进化。
Infect Immun. 2012 Dec;80(12):4061-70. doi: 10.1128/IAI.00740-12. Epub 2012 Oct 8.
6
Shigella effector IpaB-induced cholesterol relocation disrupts the Golgi complex and recycling network to inhibit host cell secretion.志贺氏菌效应蛋白 IpaB 诱导的胆固醇重定位破坏了高尔基体复合体和回收网络,从而抑制了宿主细胞的分泌。
Cell Host Microbe. 2012 Sep 13;12(3):381-9. doi: 10.1016/j.chom.2012.07.010.
7
Structurally distinct bacterial TBC-like GAPs link Arf GTPase to Rab1 inactivation to counteract host defenses.结构不同的细菌 TBC 样 GAPs 将 Arf GTPase 与 Rab1 的失活联系起来,以对抗宿主防御。
Cell. 2012 Aug 31;150(5):1029-41. doi: 10.1016/j.cell.2012.06.050.
8
Filopodium retraction is controlled by adhesion to its tip.片状伪足的回缩受其尖端附着的控制。
J Cell Sci. 2012 Nov 1;125(Pt 21):4999-5004. doi: 10.1242/jcs.104778. Epub 2012 Aug 16.
9
Shedding of genes that interfere with the pathogenic lifestyle: the Shigella model.基因的脱落会干扰致病生活方式:以志贺氏菌为例。
Res Microbiol. 2012 Jul;163(6-7):399-406. doi: 10.1016/j.resmic.2012.07.004. Epub 2012 Jul 20.
10
Hierarchies of host factor dynamics at the entry site of Shigella flexneri during host cell invasion.志贺氏菌侵袭宿主细胞过程中入侵部位宿主因子动态的层级结构。
Infect Immun. 2012 Jul;80(7):2548-57. doi: 10.1128/IAI.06391-11. Epub 2012 Apr 23.

志贺氏菌侵袭肠上皮细胞的内幕。

The inside story of Shigella invasion of intestinal epithelial cells.

机构信息

Equipe Communication Intercellulaire et Infections Microbiennes, Centre de Recherche Interdisciplinaire en Biologie (CIRB), Collège de France, Paris, France.

出版信息

Cold Spring Harb Perspect Med. 2013 Oct 1;3(10):a016717. doi: 10.1101/cshperspect.a016717.

DOI:10.1101/cshperspect.a016717
PMID:24086068
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3784809/
Abstract

As opposed to other invasive pathogens that reside into host cells in a parasitic mode, Shigella, the causative agent of bacillary dysentery, invades the colonic mucosa but does not penetrate further to survive into deeper tissues. Instead, Shigella invades, replicates, and disseminates within the colonic mucosa. Bacterial invasion and spreading in intestinal epithelium lead to the elicitation of inflammatory responses responsible for the tissue destruction and shedding in the environment for further infection of other hosts. In this article, we highlight specific features of the Shigella arsenal of virulence determinants injected by a type III secretion apparatus (T3SA) that point to the targeting of intestinal epithelial cells as a discrete route of invasion during the initial event of the infectious process.

摘要

与其他以寄生方式存在于宿主细胞内的侵袭性病原体不同,志贺氏菌是细菌性痢疾的病原体,它侵袭结肠黏膜,但不会进一步穿透以在更深的组织中存活。相反,志贺氏菌在结肠黏膜内侵袭、复制和传播。细菌入侵和在肠上皮内扩散导致引发炎症反应,导致组织破坏和脱落到环境中,以便进一步感染其他宿主。在本文中,我们强调了志贺氏菌毒力决定簇的特定特征,这些特征由 III 型分泌系统(T3SA)注入,表明在感染过程的初始事件中,针对肠上皮细胞是一种独特的入侵途径。