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本文引用的文献

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Energy Taxis toward Host-Derived Nitrate Supports a Salmonella Pathogenicity Island 1-Independent Mechanism of Invasion.能量趋向宿主来源硝酸盐支持沙门氏菌致病岛1非依赖的入侵机制。
mBio. 2016 Jul 19;7(4):e00960-16. doi: 10.1128/mBio.00960-16.
2
IgA production requires B cell interaction with subepithelial dendritic cells in Peyer's patches.IgA的产生需要B细胞与派尔集合淋巴结中的上皮下树突状细胞相互作用。
Science. 2016 May 13;352(6287):aaf4822. doi: 10.1126/science.aaf4822.
3
stg fimbrial operon from S. Typhi STH2370 contributes to association and cell disruption of epithelial and macrophage-like cells.伤寒沙门氏菌STH2370的stg菌毛操纵子有助于与上皮细胞和巨噬细胞样细胞的黏附及细胞破坏。
Biol Res. 2015 Jul 7;48(1):34. doi: 10.1186/s40659-015-0024-9.
4
Same species, different diseases: how and why typhoidal and non-typhoidal Salmonella enterica serovars differ.同一种属,不同疾病:伤寒和非伤寒沙门氏菌血清型有何不同,又是为何不同。
Front Microbiol. 2014 Aug 4;5:391. doi: 10.3389/fmicb.2014.00391. eCollection 2014.
5
Salmonella enterica Serovar Typhi conceals the invasion-associated type three secretion system from the innate immune system by gene regulation.伤寒沙门氏菌通过基因调控,向先天性免疫系统隐藏与侵袭相关的三型分泌系统。
PLoS Pathog. 2014 Jul 3;10(7):e1004207. doi: 10.1371/journal.ppat.1004207. eCollection 2014 Jul.
6
The virulence polysaccharide Vi released by Salmonella Typhi targets membrane prohibitin to inhibit T-cell activation.伤寒沙门氏菌释放的毒力多糖 Vi 靶向膜抑素以抑制 T 细胞活化。
J Infect Dis. 2014 Jul 1;210(1):79-88. doi: 10.1093/infdis/jiu064. Epub 2014 Jan 26.
7
The delicate balance in genetically engineering live vaccines.基因工程活疫苗中的微妙平衡。
Vaccine. 2014 Jul 31;32(35):4376-4385. doi: 10.1016/j.vaccine.2013.12.026. Epub 2013 Dec 23.
8
Typhoid fever and paratyphoid fever: Systematic review to estimate global morbidity and mortality for 2010.伤寒和副伤寒:系统评价估计 2010 年全球发病率和死亡率。
J Glob Health. 2012 Jun;2(1):010401. doi: 10.7189/jogh.02.010401.
9
Host-pathogen interaction in invasive Salmonellosis.宿主-病原体相互作用在侵袭性沙门氏菌病中的作用。
PLoS Pathog. 2012;8(10):e1002933. doi: 10.1371/journal.ppat.1002933. Epub 2012 Oct 4.
10
Phage-mediated acquisition of a type III secreted effector protein boosts growth of salmonella by nitrate respiration.噬菌体介导获得 III 型分泌效应蛋白通过硝酸盐呼吸促进沙门氏菌生长。
mBio. 2012 Jun 12;3(3). doi: 10.1128/mBio.00143-12. Print 2012.

长极菌毛和Stg菌毛在沙门氏菌与肠上皮细胞和M细胞相互作用中作用的新见解

New Insights into the Roles of Long Polar Fimbriae and Stg Fimbriae in Salmonella Interactions with Enterocytes and M Cells.

作者信息

Gonzales Amanda M, Wilde Shyra, Roland Kenneth L

机构信息

Biodesign Institute, Arizona State University, Tempe, Arizona, USA.

Biodesign Institute, Arizona State University, Tempe, Arizona, USA

出版信息

Infect Immun. 2017 Aug 18;85(9). doi: 10.1128/IAI.00172-17. Print 2017 Sep.

DOI:10.1128/IAI.00172-17
PMID:28630073
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5563581/
Abstract

serovar Typhi causes the systemic disease typhoid fever. After ingestion, it adheres to and invades the host epithelium while evading the host innate immune response, causing little if any inflammation. Conversely, serovar Typhimurium causes gastroenteritis in humans and thrives in the inflamed gut. Upon entering the host, Typhimurium preferentially colonizes Peyer's patches, a lymphoid organ in which microfold cells (M cells) overlay an arrangement of B cells, T cells, and antigen-presenting cells. Both serovars can adhere to and invade M cells and enterocytes, and it has been assumed that Typhi also preferentially targets M cells. In this study, we present data supporting the alternative hypothesis that Typhi preferentially targets enterocytes. Using a tissue culture M cell model, we examined Typhi strains with a deletion in the fimbriae. The deletion resulted in increased adherence to M cells and, as expected, decreased adherence to Caco-2 cells. Adherence to M cells could be further enhanced by introduction of the long polar fimbriae (Lpf), which facilitate adherence of Typhimurium to M cells. Deletion of and/or introduction of enhanced M cell invasion as well, leading to significant increases in secretion of interleukin 8. These results suggest that Typhi may preferentially target enterocytes .

摘要

伤寒杆菌会引发全身性疾病伤寒热。摄入后,它会黏附并侵入宿主上皮细胞,同时逃避宿主的固有免疫反应,几乎不会引发炎症(即便有炎症也很轻微)。相反,鼠伤寒杆菌会导致人类患肠胃炎,并在发炎的肠道中大量繁殖。进入宿主后,鼠伤寒杆菌优先定殖于派尔集合淋巴结,这是一种淋巴器官,其中微褶细胞(M细胞)覆盖着B细胞、T细胞和抗原呈递细胞的排列结构。两种血清型都能黏附并侵入M细胞和肠上皮细胞,并且一直以来人们认为伤寒杆菌也优先靶向M细胞。在本研究中,我们提供的数据支持了另一种假说,即伤寒杆菌优先靶向肠上皮细胞。我们使用组织培养的M细胞模型,检测了菌毛缺失的伤寒杆菌菌株。这种缺失导致对M细胞的黏附增加,并且正如预期的那样,对Caco-2细胞的黏附减少。引入长极菌毛(Lpf)可进一步增强对M细胞的黏附,长极菌毛有助于鼠伤寒杆菌黏附于M细胞。菌毛的缺失和/或引入也增强了对M细胞的侵袭,导致白细胞介素8的分泌显著增加。这些结果表明,伤寒杆菌可能优先靶向肠上皮细胞。