文献类型：期刊文献

英文题名：PurA facilitates Edwardsiella piscicida to escape NF-KB signaling activation

作者：Hu, Feizi[1];Zhang, Yuanxing[2,3];Liu, Qin[1,2,3];Wang, Zhuang[1]

机构：[1]East China Univ Sci & Technol, State Key Lab Bioreactor Engn, Shanghai 200237, Peoples R China;[2]Southern Marine Sci & Engn Guangdong Lab Zhuhai, Zhuhai 519000, Peoples R China;[3]Shanghai Engn Res Ctr Maricultured Anim Vaccines, Shanghai 200237, Peoples R China

年份：2022

卷号：124

起止页码：254

外文期刊名：FISH & SHELLFISH IMMUNOLOGY

收录：;WOS:【SCI-EXPANDED(收录号:WOS:000798809000004)】；

基金：Acknowledgements This work was supported by the National Natural Science Foundation of China No. 32025038 (Q.L.) , the Innovation Group Project of Southern Marine Science and Engineering Guangdong Laboratory (Zhuhai) (311020005) , and the Fundamental Research Funds for the Central Universities (222201211729) .

语种：英文

外文关键词：Edwardsiella piscicida; Adenylosuccinate synthase; NF-KB singlaing; Immuno-evasion

摘要：The host NF-KB signaling pathway plays critical role in defensing against bacterial infection. However, bacteria also evolve strategies to escape from host clearance. Edwardsiella piscicida is a threatening pathogen in aquaculture, while the molecular mechanism of E. piscicida in inhibiting NF-KB signaling remains largely unknown. Herein, using E. piscicida transposon insertion mutant library combined with a NF-KB luciferase reporter system, we identified forty-six genes of E. piscicida, which were involved in inhibiting the NF-KB signaling activation in vitro. Moreover, we further explored the top 10 significantly changed mutants through zebrafish larvae infection model and validated that six genes were involved in inhibiting NF-KB activation in vivo. Specifically, we identified the adenylosuccinate synthase mutated strain (Delta purA) infection exhibited a robust activation of NF-KB signaling, along with higher expression of cxcl8a and cxcl8b to mediate the recruitment of neutrophils in vivo. Taken together, these results identified the key factors of E. piscicida in inhibiting NF-KB activation, which will contribute to better understanding the pathogenesis of this important pathogen.