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Function of Rhs proteins in porcine extraintestinal pathogenic Escherichia coli PCN033

文献类型： 外文期刊

作者： Lu, Wenjia 1 ; Tan, Jia 3 ; Lu, Hao 1 ; Wang, Gaoyan 1 ; Dong, Wenqi 1 ; Wang, Chenchen 1 ; Li, Xiaodan 1 ; Tan, Chen 1 ;

作者机构： 1.Huazhong Agr Univ, Coll Vet Med, State Key Lab Agr Microbiol, Wuhan 430070, Peoples R China

2.Cooperat Innovat Ctr Sustainable Pig Prod, Key Lab Prevent Vet Med Hubei Prov, Wuhan 430040, Peoples R China

3.Jiangxi Acad Agr Sci, Shangrao 333104, Jiangxi, Peoples R China

关键词： type VI secretion system; rearrangement hotspot; pathogenicity; virulence; anti-phagocytosis; ExPEC

期刊名称：JOURNAL OF MICROBIOLOGY （ 影响因子：3.422； 五年影响因子：3.28 ）

ISSN： 1225-8873

年卷期： 2021 年 59 卷 9 期

页码：

收录情况： SCI

摘要： Extraintestinal pathogenic Escherichia coli (ExPEC) is an important zoonotic pathogen that places severe burdens on public health and animal husbandry. There are many pathogenic factors in E. coli. The type VI secretion system (T6SS) is a nano-microbial weapon that can assemble quickly and inject toxic effectors into recipient cells when danger is encountered. T6SSs are encoded in the genomes of approximately 25% of sequenced Gram-negative bacteria. When these bacteria come into contact with eukaryotic cells or prokaryotic microbes, the T6SS assembles and secretes associated effectors. In the porcine ExPEC strain PCN033, we identified four classic rearrangement hotspot (Rhs) genes. We determined the functions of the four Rhs proteins through mutant construction and protein expression. Animal infection experiments showed that the Delta rhs-1CT, Delta rhs-2CT, Delta rhs-3CT, and Delta rhs-4CT caused a significant decrease in the multiplication ability of PCN033 in vivo. Cell infection experiments showed that the Rhs protein is involved in anti-phagocytosis activities and bacterial adhesion and invasion abilities. The results of this study demonstrated that rhs1, rhs3, and rh4 plays an important role in the interaction between PCN033 and host cell. Rhs2 has contribution to cell and mice infection. This study helps to elucidate the pathogenic mechanism governing PCN033 and may help to establish a foundation for further research seeking to identify potential T6SS effectors.

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