Title Function of Rhs proteins in porcine extraintestinal pathogenic Escherichia coli PCN033
Author Wenjia Lu1,2, Jia Tan3, Hao Lu1,2, Gaoyan Wang1,2, Wenqi Dong1,2, Chenchen Wang1,2, Xiaodan Li1,2, and Chen Tan1,2*
Address 1State Key Laboratory of Agricultural Microbiology, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan 430070, P. R. China, 2Key Laboratory of Preventive Veterinary Medicine in Hubei Province, The Cooperative Innovation Center for Sustainable Pig Production, Wuhan 430040, P. R. China, 3Jiangxi Academy of Agricultural Science, Jiangxi 333104, P.R. China
Bibliography Journal of Microbiology, 59(9),854-860, 2021,
DOI 10.1007/s12275-021-1189-2
Key Words type VI secretion system, rearrangement hotspot, pathogenicity, virulence, anti-phagocytosis, ExPEC
Abstract 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 Δrhs-1CT, Δrhs-2CT, Δrhs-3CT, and Δrhs-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.