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对肠致病性大肠杆菌E2348/69的 和 进行双突变会减弱其毒力并诱导白细胞介素6产生。 （注：原文中“both and ”部分缺失具体内容）

Mutating both and of enteropathogenic E2348/69 attenuates its virulence and induces interleukin 6 .

作者信息

Lee Jun Bong, Kim Se Kye, Han Dalmuri, Yoon Jang Won

机构信息

College of Veterinary Medicine, Institute of Veterinary Science, Kangwon National University, Chuncheon, Gangwon, Republic of Korea.

出版信息

Front Microbiol. 2023 Mar 2;14:1121715. doi: 10.3389/fmicb.2023.1121715. eCollection 2023.

DOI:10.3389/fmicb.2023.1121715
PMID:36937293
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10017862/
Abstract

Here, we report for the first time that disrupting both and genes in enteropathogenic E2348/69 can attenuate its virulence and significantly induce interleukin 6 (IL-6) . Our experimental analyses demonstrated that an E2348/69 ΔΔ double mutant strain derepressed the expression of type IV bundle forming pilus (BFP) and repressed the expression of glutamate decarboxylase (GAD) and locus of enterocyte effacement (LEE). Whole genome-scale transcriptomic analysis revealed that 1,564 EPEC genes were differentially expressed in the ΔΔ double mutant strain (cut-off > two-fold). Such depletion of and attenuated the virulence of E2348/69 in a infection model. Surprisingly, IL-6 was highly induced in porcine macrophages infected with the ΔΔ double mutant strain compared to those with its wildtype strain. Coinciding with these results, murine peritoneal challenge assays showed high increase of IL-6 and improved bacterial clearance in response to infection by the ΔΔ double mutant strain. Taken together, our data suggest that and play an essential role in regulating biological processes during EPEC pathogenesis and that their depletion can affect host immune responses by inducing IL-6.

摘要

在此，我们首次报道，破坏肠致病性大肠杆菌E2348/69中的 和 基因可减弱其毒力并显著诱导白细胞介素6（IL-6）。我们的实验分析表明，E2348/69 ΔΔ双突变菌株抑制了IV型束状菌毛（BFP）的表达，并抑制了谷氨酸脱羧酶（GAD）和肠上皮细胞损伤位点（LEE）的表达。全基因组规模的转录组分析显示，1564个EPEC基因在ΔΔ双突变菌株中差异表达（截止值>两倍）。 和 的这种缺失在 感染模型中减弱了E2348/69的毒力。令人惊讶的是，与野生型菌株相比，感染ΔΔ双突变菌株的猪巨噬细胞中IL-6被高度诱导。与这些结果一致，小鼠腹腔攻击试验显示，响应于ΔΔ双突变菌株的感染，IL-6显著增加且细菌清除得到改善。综上所述，我们的数据表明， 和 在EPEC发病机制的生物学过程调节中起重要作用，并且它们的缺失可通过诱导IL-6影响宿主免疫反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c63c/10017862/c82f0656dcf5/fmicb-14-1121715-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c63c/10017862/03c88481e3e4/fmicb-14-1121715-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c63c/10017862/6ccb6ffd8eec/fmicb-14-1121715-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c63c/10017862/00970afe9027/fmicb-14-1121715-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c63c/10017862/5d7c4b709d35/fmicb-14-1121715-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c63c/10017862/63532ce034fc/fmicb-14-1121715-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c63c/10017862/5f2c8f604d37/fmicb-14-1121715-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c63c/10017862/04ad44cd752b/fmicb-14-1121715-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c63c/10017862/f9440361a9eb/fmicb-14-1121715-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c63c/10017862/c82f0656dcf5/fmicb-14-1121715-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c63c/10017862/03c88481e3e4/fmicb-14-1121715-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c63c/10017862/6ccb6ffd8eec/fmicb-14-1121715-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c63c/10017862/00970afe9027/fmicb-14-1121715-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c63c/10017862/5d7c4b709d35/fmicb-14-1121715-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c63c/10017862/63532ce034fc/fmicb-14-1121715-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c63c/10017862/5f2c8f604d37/fmicb-14-1121715-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c63c/10017862/04ad44cd752b/fmicb-14-1121715-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c63c/10017862/f9440361a9eb/fmicb-14-1121715-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c63c/10017862/c82f0656dcf5/fmicb-14-1121715-g009.jpg

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