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Regulation of ydiV-induced biological characteristics permits Escherichia coli evasion of the host STING inflammatory response
Veterinary Microbiology ( IF 3.3 ) Pub Date : 2021-08-14 , DOI: 10.1016/j.vetmic.2021.109207
Xudong Wang 1 , Xinguang Lin 1 , Zhixin Wan 1 , Jiakun Zuo 2 , Zhihao Wang 3 , Yuanyuan Xu 1 , Vanhnaseng Phouthapane 4 , Xiangan Han 3 , Jinqiu Zhang 5 , Jinfeng Miao 1
Affiliation  

Mammary gland-derived Escherichia coli (E. coli) is an important pathogen causing dairy cow mastitis. YdiV, with EAL-like domains, inhibits flagellum biogenesis and motility and affects c-di-GMP (eubacterial signaling molecule) concentration changes in bacteria. However, the pathophysiological role of ydiV in host-pathogen cross-talk still needs to be elucidated. In this study, firstly constructed the ydiV mutant (NJ17ΔydiV) and ydiV complementary (cNJ17ΔydiV) E. coli strains to infect mouse mammary epithelial cells (EpH4-Ev) and macrophages (RAW264.7), as well as mouse mammary glands, respectively. Then biological characteristics, adaptor molecules in related signaling pathways, proinflammatory cytokines and the extent of host cell damage was evaluated. Compared with E. coli NJ17 infected mice, the bacterial load in the mammary gland of NJ17ΔydiV was significantly lower and the extent of the damage was alleviated. Notably, the deletion of ydiV significantly aggravated cell damage in RAW264.7 cells and compared with the wild-type strain, NJ17ΔydiV significantly activated the STING/TBK1/IRF3 pathway in macrophages. In EpH4-Ev cells, although STING did not sense E. coli NJ17 invasion, IRF3 was activated by the NJ17ΔydiV strain. Taken together, ydiV deletion significantly affects a variety of biological characteristics and induces severe cell damage, while the STING/TBK1/IRF3 pathway actively participated in pathogen elimination in the host. This study highlights a new role for ydiV in E. coli infection and provides a foundation for further studies to better understand host-bacteria interactions and potential prophylactic strategies for infectious diseases.



中文翻译:

ydiV 诱导的生物学特性的调节允许大肠杆菌逃避宿主 STING 炎症反应

乳腺源性大肠杆菌E.coli)是引起奶牛乳腺炎的重要病原体。YdiV 具有 EAL 样结构域,可抑制鞭毛生物发生和运动,并影响细菌中的 c-di-GMP(真细菌信号分子)浓度变化。然而,ydiV在宿主-病原体串扰中的病理生理作用仍有待阐明。本研究首先构建了ydiV突变体(NJ17Δ ydiV)和ydiV互补(cNJ17Δ ydiV大肠杆菌分别感染小鼠乳腺上皮细胞 (EpH4-Ev) 和巨噬细胞 (RAW264.7) 以及小鼠乳腺的菌株。然后评估生物学特性、相关信号通路中的衔接分子、促炎细胞因子和宿主细胞损伤的程度。与大肠杆菌NJ17 感染的小鼠相比,NJ17Δ ydiV乳腺中的细菌载量显着降低,损伤程度有所减轻。值得注意的是,ydiV的缺失显着加剧了 RAW264.7 细胞的细胞损伤,与野生型菌株相比,NJ17Δ ydiV显着激活了巨噬细胞中的 STING/TBK1/IRF3 通路。在 EpH4-Ev 细胞中,虽然 STING 没有感知到大肠杆菌NJ17 入侵,IRF3 被 NJ17Δ ydiV菌株激活。综上所述,ydiV缺失显着影响多种生物学特性并诱导严重的细胞损伤,而 STING/TBK1/IRF3 通路积极参与宿主中的病原体消除。这项研究突出了ydiV大肠杆菌感染中的新作用,并为进一步研究以更好地了解宿主-细菌相互作用和传染病的潜在预防策略奠定了基础。

更新日期:2021-08-19
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