Suppr超能文献

肠致病性大肠杆菌对肠出血性大肠杆菌感染的交叉保护作用在小鼠模型中的研究。

Cross-reactive protection against enterohemorrhagic Escherichia coli infection by enteropathogenic E. coli in a mouse model.

机构信息

Department of Pediatrics, Clinical Sciences Lund, Lund University, 22185 Lund, Sweden.

出版信息

Infect Immun. 2011 Jun;79(6):2224-33. doi: 10.1128/IAI.01024-10. Epub 2011 Mar 14.

Abstract

Enteropathogenic Escherichia coli (EPEC) and enterohemorrhagic E. coli (EHEC) are related attaching and effacing (A/E) pathogens. The genes responsible for the A/E pathology are carried on a chromosomal pathogenicity island termed the locus of enterocyte effacement (LEE). Both pathogens share a high degree of homology in the LEE and additional O islands. EHEC prevalence is much lower in areas where EPEC is endemic. This may be due to the development of antibodies against common EPEC and EHEC antigens. This study investigated the hypothesis that EPEC infections may protect against EHEC infections. We used a mouse model to inoculate BALB/c mice intragastrically, first with EPEC and then with EHEC (E. coli O157:H7). Four control groups received either a nonpathogenic E. coli (NPEC) strain followed by EHEC (NPEC/EHEC), phosphate-buffered saline (PBS) followed by EHEC (PBS/EHEC), EPEC/PBS, or PBS/PBS. Mice were monitored for weight loss and symptoms. EPEC colonized the intestine after challenge, and mice developed serum antibodies to intimin and E. coli secreted protein B (encoded in the LEE). Prechallenge with an EPEC strain had a protective effect after EHEC infection, as only a few mice developed mild symptoms, from which they recovered. These mice had an increase in body weight similar to that in control animals, and tissue morphology exhibited mild intestinal changes and normal renal histology. All mice that were not prechallenged with the EPEC strain developed mild to severe symptoms after EHEC infection, with weight loss as well as intestinal and renal histopathological changes. These data suggest that EPEC may protect against EHEC infection in this mouse model.

摘要

肠致病性大肠杆菌(EPEC)和肠出血性大肠杆菌(EHEC)是相关的黏附性和破坏性(A/E)病原体。负责 A/E 病理学的基因位于一个被称为肠细胞消失(LEE)的染色体致病性岛(pathogenicity island)上。两种病原体在 LEE 和其他 O 岛方面具有高度同源性。在 EPEC 流行的地区,EHEC 的流行率要低得多。这可能是由于针对常见 EPEC 和 EHEC 抗原的抗体的发展。本研究旨在调查 EPEC 感染可能对 EHEC 感染具有保护作用的假说。我们使用小鼠模型,通过胃内接种首先将 BALB/c 小鼠接种 EPEC,然后接种 EHEC(E. coli O157:H7)。四个对照组分别接受非致病性大肠杆菌(NPEC)株,然后接种 EHEC(NPEC/EHEC),磷酸盐缓冲盐水(PBS),然后接种 EHEC(PBS/EHEC),EPEC/PBS 或 PBS/PBS。监测小鼠的体重减轻和症状。EPEC 在受到挑战后定植于肠道,并且小鼠产生针对 intimine 和大肠杆菌分泌蛋白 B(在 LEE 中编码)的血清抗体。在 EHEC 感染前用 EPEC 株进行预挑战具有保护作用,因为只有少数小鼠出现轻度症状,并且从这些症状中恢复。这些小鼠的体重增加与对照动物相似,组织形态学显示出轻度的肠道变化和正常的肾脏组织学。所有未用 EPEC 株进行预挑战的小鼠在感染 EHEC 后均出现轻度至重度症状,伴有体重减轻以及肠道和肾脏组织病理学变化。这些数据表明,在这种小鼠模型中,EPEC 可能对 EHEC 感染具有保护作用。

相似文献

1
2

引用本文的文献

2
Red blood cell-derived arginase release in hemolytic uremic syndrome.
J Transl Med. 2024 Jan 4;22(1):17. doi: 10.1186/s12967-023-04824-x.
3
Detection and analysis of Shiga toxin producing and enteropathogenic Escherichia coli in cattle from Tierra del Fuego, Argentina.
Braz J Microbiol. 2023 Jun;54(2):1257-1266. doi: 10.1007/s42770-023-00958-8. Epub 2023 Apr 11.
4
The Diversity of Pathotypes and Vaccination Strategies against This Versatile Bacterial Pathogen.
Microorganisms. 2023 Jan 30;11(2):344. doi: 10.3390/microorganisms11020344.
5
Diagnosis and Treatment for Shiga Toxin-Producing Associated Hemolytic Uremic Syndrome.
Toxins (Basel). 2022 Dec 23;15(1):10. doi: 10.3390/toxins15010010.
6
7
Oral Administration with Live Attenuated Citrobacter rodentium Protects Immunocompromised Mice from Lethal Infection.
Infect Immun. 2022 Jul 21;90(7):e0019822. doi: 10.1128/iai.00198-22. Epub 2022 Jul 5.
8
AB Enterotoxin-Mediated Pathogenesis: Perspectives Gleaned from Shiga Toxins.
Toxins (Basel). 2022 Jan 16;14(1):62. doi: 10.3390/toxins14010062.
9
Annexin Induces Cellular Uptake of Extracellular Vesicles and Delays Disease in O157:H7 Infection.
Microorganisms. 2021 May 26;9(6):1143. doi: 10.3390/microorganisms9061143.
10
as a Multifaceted Pathogenic and Versatile Bacterium.
Front Cell Infect Microbiol. 2020 Dec 21;10:548492. doi: 10.3389/fcimb.2020.548492. eCollection 2020.

本文引用的文献

1
Endotoxin tolerance: new mechanisms, molecules and clinical significance.
Trends Immunol. 2009 Oct;30(10):475-87. doi: 10.1016/j.it.2009.07.009. Epub 2009 Sep 24.
2
Shiga toxin-mediated disease in MyD88-deficient mice infected with Escherichia coli O157:H7.
Am J Pathol. 2008 Nov;173(5):1428-39. doi: 10.2353/ajpath.2008.071218. Epub 2008 Oct 2.
4
Reduced virulence of an fliC mutant of Shiga-toxigenic Escherichia coli O113:H21.
Infect Immun. 2006 Mar;74(3):1962-6. doi: 10.1128/IAI.74.3.1962-1966.2006.
5
A comparison of enteropathogenic and enterohaemorrhagic Escherichia coli pathogenesis.
FEMS Microbiol Lett. 2006 Feb;255(2):187-202. doi: 10.1111/j.1574-6968.2006.00119.x.
7
Evolution of genomic content in the stepwise emergence of Escherichia coli O157:H7.
J Bacteriol. 2005 Mar;187(5):1783-91. doi: 10.1128/JB.187.5.1783-1791.2005.

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验