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本文引用的文献

1
Proteomic Analysis of IPEC-J2 Cells in Response to Coinfection by Porcine Transmissible Gastroenteritis Virus and Enterotoxigenic Escherichia coli K88.猪传染性胃肠炎病毒与产肠毒素大肠杆菌K88共感染后IPEC-J2细胞的蛋白质组学分析
Proteomics Clin Appl. 2017 Dec;11(11-12). doi: 10.1002/prca.201600137.
2
Persistent Transmissible Gastroenteritis Virus Infection Enhances Enterotoxigenic Escherichia coli K88 Adhesion by Promoting Epithelial-Mesenchymal Transition in Intestinal Epithelial Cells.持续性传染性胃肠炎病毒感染通过促进肠上皮细胞的上皮-间质转化增强产肠毒素大肠杆菌K88的黏附。
J Virol. 2017 Oct 13;91(21). doi: 10.1128/JVI.01256-17. Print 2017 Nov 1.
3
Stress, Nutrition, and Intestinal Immune Responses in Pigs - A Review.猪的应激、营养与肠道免疫反应——综述
Asian-Australas J Anim Sci. 2016 Aug;29(8):1075-82. doi: 10.5713/ajas.16.0118. Epub 2016 May 12.
4
Comparing Two Intestinal Porcine Epithelial Cell Lines (IPECs): Morphological Differentiation, Function and Metabolism.比较两种猪肠道上皮细胞系(IPECs):形态分化、功能与代谢
PLoS One. 2015 Jul 6;10(7):e0132323. doi: 10.1371/journal.pone.0132323. eCollection 2015.
5
Macrophage cytokines: involvement in immunity and infectious diseases.巨噬细胞细胞因子:在免疫和传染病中的作用。
Front Immunol. 2014 Oct 7;5:491. doi: 10.3389/fimmu.2014.00491. eCollection 2014.
6
Several enteropathogens are circulating in suckling and newly weaned piglets suffering from diarrhea in the province of Villa Clara, Cuba.在古巴比那尔德里奥省,几种肠道病原体在患有腹泻的哺乳仔猪和刚断奶仔猪中传播。
Trop Anim Health Prod. 2013 Feb;45(2):435-40. doi: 10.1007/s11250-012-0236-8. Epub 2012 Jul 29.
7
Synergistic effects between rotavirus and coinfecting pathogens on diarrheal disease: evidence from a community-based study in northwestern Ecuador.轮状病毒与合并感染病原体对腹泻病的协同作用:来自厄瓜多尔西北部一项基于社区的研究证据。
Am J Epidemiol. 2012 Sep 1;176(5):387-95. doi: 10.1093/aje/kws220. Epub 2012 Jul 25.
8
LC3 and GATE-16/GABARAP subfamilies are both essential yet act differently in autophagosome biogenesis.LC3 和 GATE-16/GABARAP 亚家族在自噬体生物发生中都是必不可少的,但作用方式不同。
EMBO J. 2010 Jun 2;29(11):1792-802. doi: 10.1038/emboj.2010.74. Epub 2010 Apr 23.
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Frequent expression of Niban in head and neck squamous cell carcinoma and squamous dysplasia.Niban 在头颈部鳞状细胞癌和鳞状发育不良中频繁表达。
Head Neck. 2010 Jan;32(1):96-103. doi: 10.1002/hed.21153.
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Enterotoxigenic Escherichia coli modulates host intestinal cell membrane asymmetry and metabolic activity.产肠毒素大肠杆菌调节宿主肠道细胞膜不对称性和代谢活性。
Infect Immun. 2009 Jan;77(1):341-7. doi: 10.1128/IAI.01097-08. Epub 2008 Oct 20.

从蛋白质组学角度理解猪传染性胃肠炎病毒-产肠毒素大肠杆菌混合感染:猪腹泻的故事

Understanding TGEV-ETEC Coinfection through the Lens of Proteomics: A Tale of Porcine Diarrhea.

作者信息

Arango Duque Guillermo, Acevedo Ospina Hamlet Adolfo

机构信息

INRS-Institut Armand-Frappier and Centre for Host-Parasite Interactions, Laval, QC, Canada.

出版信息

Proteomics Clin Appl. 2018 May;12(3):e1700143. doi: 10.1002/prca.201700143. Epub 2018 Jan 31.

DOI:10.1002/prca.201700143
PMID:29281177
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7167695/
Abstract

Porcine diarrhea and gastroenteritis are major causes of piglet mortality that result in devastating economic losses to the industry. A plethora of pathogens can cause these diseases, with the transmissible gastroenteritis virus (TGEV) and enterotoxigenic Escherichia coli K88 (ETEC) being two of the most salient. In the December 2017 issue of Proteomics Clinical Aplications, Xia and colleagues used comparative proteomics to shed light on how these microbes interact to cause severe disease . The authors discovered that TGEV induces an epithelial-mesenchymal transition-like phenotype that augments cell adhesion proteins mediating the attachment of ETEC to intestinal epithelial cells. Moreover, coinfection was found to modulate several host proteins that could bolster pathogen persistence. Importantly, the authors observed that ETEC suppresses the production of inflammatory cytokines induced by TGEV, which may in turn promote the long-term survival of both microbes.

摘要

猪腹泻和肠胃炎是导致仔猪死亡的主要原因,给养猪业造成了巨大的经济损失。大量病原体可引发这些疾病,其中传染性肠胃炎病毒(TGEV)和产肠毒素大肠杆菌K88(ETEC)是最突出的两种。在2017年12月的《蛋白质组学临床应用》杂志上,夏及其同事运用比较蛋白质组学来阐明这些微生物如何相互作用导致严重疾病。作者发现,TGEV诱导出一种上皮-间质转化样表型,增强了介导ETEC附着于肠道上皮细胞的细胞粘附蛋白。此外,发现共感染会调节几种宿主蛋白,这些蛋白可能会增强病原体的持久性。重要的是,作者观察到ETEC抑制了TGEV诱导的炎性细胞因子的产生,这反过来可能会促进两种微生物的长期存活。