Intestinal microbiota mediates Enterotoxigenic Escherichia coli-induced diarrhea in piglets

Intestinal microbiota mediates Enterotoxigenic Escherichia coli-induced diarrhea in piglets
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肠道微生物群介导产肠毒素大肠杆菌引起的仔猪腹泻

DOI:
10.1186/s12917-018-1704-9
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发表时间:
2018-12-05
影响因子:
2.6
通讯作者:
Zhu, Guoqiang
Zhu, Guoqiang
中科院分区:
农林科学2区
文献类型:
--
作者:
Bin, Peng;Tang, Zhiyi;Zhu, Guoqiang

文献摘要

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背景:产肠毒素大肠杆菌(ETEC)可引起人、牛和猪的腹泻。肠道微生物区系是几种感染性疾病的病理基础,但肠道微生物区系在ETEC诱导的腹泻发病机制中的作用尚不清楚。结果:通过ETEC诱导的仔猪腹泻模型,我们用元基因组学和16S rRNA测序的方法描述了空肠和粪便的微生物区系。进行了空肠微生物区系移植实验,以确定肠道微生物区系在ETEC诱导的腹泻中的作用。ETEC诱导的腹泻影响肠道微生物区系的结构和功能。腹泻仔猪空肠和粪便中类杆菌:菌落比和微生物区系多样性较低,粪便中普氏杆菌百分率较低,空肠中乳球菌和粪便中的乳杆菌较高,粪便中的大肠杆菌较高。将腹泻仔猪的空肠微生物区系移植到未感染的仔猪身上,导致移植后的腹泻。微生物区系移植实验也支持肠道微生物区系失调参与ETEC所致腹泻免疫应答的观点。结论:ETEC感染影响肠道微生物区系,ETEC感染后肠道微生物区系失调介导了ETEC感染的免疫应答。
Background:Enterotoxigenic Escherichia coli (ETEC) causes diarrhea in humans, cows, and pigs. The gut microbiota underlies pathology of several infectious diseases yet the role of the gut microbiota in the pathogenesis of ETEC-induced diarrhea is unknown.Results:By using an ETEC induced diarrheal model in piglet, we profiled the jejunal and fecal microbiota using metagenomics and 16S rRNA sequencing. A jejunal microbiota transplantation experiment was conducted to determine the role of the gut microbiota in ETEC-induced diarrhea. ETEC-induced diarrhea influenced the structure and function of gut microbiota. Diarrheal piglets had lower Bacteroidetes: Firmicutes ratio and microbiota diversity in the jejunum and feces, and lower percentage of Prevotella in the feces, but higher Lactococcus in the jejunum and higher Escherichia-Shigella in the feces. The transplantation of the jejunal microbiota from diarrheal piglets to uninfected piglets leaded to diarrhea after transplantation. Microbiota transplantation experiments also supported the notion that dysbiosis of gut microbiota is involved in the immune responses in ETEC-induced diarrhea.Conclusion:We conclude that ETEC infection influences the gut microbiota and the dysbiosis of gut microbiota after ETEC infection mediates the immune responses in ETEC infection.