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P25 对肠产毒性 K88 感染的保护作用及其潜在机制的转录组学分析。

P25 Protected against Enterotoxigenic K88 Infection and Transcriptomic Analysis of Its Potential Mechanisms.

机构信息

Institute of Animal Science, Guangdong Academy of Agricultural Sciences, State Key Laboratory of Livestock and Poultry Breeding, The Key Laboratory of Animal Nutrition and Feed Science (South China) of Ministry of Agriculture, Guangdong Key Laboratory of Animal Breeding and Nutrition, Guangdong Engineering Technology Research Center of Animal Meat Quality and Safety Control and Evaluation, Guangzhou, China 510640.

出版信息

Biomed Res Int. 2020 Mar 30;2020:7340312. doi: 10.1155/2020/7340312. eCollection 2020.

Abstract

Enterotoxigenic (ETEC) K88 is a zoonotic pathogen. Previous studies have shown that lactic acid bacteria (LAB) have great potential in promoting health and resisting pathogenic infections; however, relatively little research has been done on the genus of LAB. This study is aimed at exploring the mechanisms imparted by P25 against ETEC K88 in . The probiotic performance of P25 was investigated in vitro. Colonization of K88 in the intestinal tract of . and abundance of enterotoxin genes were measured. In addition, the transcriptome of . infected by K88 was analyzed. The result showed that P25 possessed the ability to produce acid, as well as high tolerances to acidic and high bile salt concentrations. Coculture revealed that the growth of ETEC K88 was significantly inhibited by the presence of P25. The median survival of . fed P25 was 2 days longer than the group infected with K88 alone ( < 0.01). At the same time, the number of colonizing K88 and the abundances of and were reduced by up to 71.70% and 2.17 times, respectively, by P25. Transcriptome data indicated that P25 affected expression of genes relative to innate immune response and upregulated the abundance of genes in multiple pathways of . , including peroxisome, longevity, and mitogen-activated protein kinase (MAPK) pathways. These results demonstrated that in the presence of P25, K88 colonization and their expression of enterotoxin genes were reduced. This was accomplished through the alteration of environmental parameters (pH and bile salt) as well as through the promotion of the innate immune response processes, increased longevity, and increased antipathogenic bacteria-related pathways. This work highlights the potential application of . P25 as a probiotic resistant to ETEC K88.

摘要

产肠毒素性(ETEC)K88 是一种人畜共患病病原体。先前的研究表明,乳酸菌(LAB)在促进健康和抵抗病原感染方面具有巨大的潜力;然而,关于 LAB 属的研究相对较少。本研究旨在探索 P25 对 ETEC K88 的作用机制。在体外研究了 P25 的益生菌性能。测量了 K88 在. 肠道中的定植和肠毒素基因的丰度。此外,还分析了 K88 感染. 的转录组。结果表明,P25 具有产酸能力,并且能够耐受酸性和高胆汁盐浓度。共培养表明,ETEC K88 的生长受到 P25 的显著抑制。用 P25 喂养的. 的中位存活时间比单独感染 K88 的组长 2 天(<0.01)。同时,P25 使定植 K88 的数量和. 和 的丰度分别减少了 71.70%和 2.17 倍。转录组数据表明,P25 影响了与先天免疫反应相关的基因的表达,并上调了. 中多个途径的基因丰度,包括过氧化物酶体、长寿和丝裂原活化蛋白激酶(MAPK)途径。这些结果表明,在 P25 的存在下,K88 的定植及其肠毒素基因的表达减少。这是通过改变环境参数(pH 和胆汁盐)以及促进先天免疫反应过程、增加长寿和增加抗病原细菌相关途径来实现的。这项工作强调了. P25 作为一种抗 ETEC K88 的益生菌的潜在应用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0432/7150717/193663f55a09/BMRI2020-7340312.001.jpg

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