TLR5b-mediated NF-KB activation promotes neutrophil recruitment to defense Edwardsiella piscicida infection in zebrafish

被引:0
|
作者
Hu, Feizi [1 ]
Wang, Zhuang [1 ]
Zhang, Yuanxing [2 ,3 ]
Yang, Dahai [1 ,3 ]
Liu, Qin [1 ,3 ]
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
基金
中国国家自然科学基金;
关键词
Edwardsiella piscicida; NF-KB; TLR5b; Neutrophil; Zebrafish; TOLL-LIKE RECEPTORS; KAPPA-B; CHANNEL CATFISH; T-CELLS; EXPRESSION; FISH; TLR; PATHWAYS; DELETION; ALPHA;
D O I
10.1016/j.aquaculture.2022.739041
中图分类号
S9 [水产、渔业];
学科分类号
0908 ;
摘要
NF -KB signaling pathway plays important roles in innate immunity, which could response to various microbials infection and mediate immune defense. It has been reported that NF -KB signaling could be activated after Edwardsiella piscicida infection in zebrafish, while the molecular mechanism of NF -KB signaling in defensing against E. piscicida remains largely unknown. Herein, we use an in vivo NF -KB detection model in larvae, and confirm that the NF -KB signaling pathway was activated by upstream receptor TLR5b through recognizing the flagella of E. piscicida. Besides, we explore the expression of immune-related genes which regulated by NF -KB during infection. Specifically, NF -KB activation upregulates the expression of cxcl8a, promoting the recruitment of neutrophils. Moreover, we prove that NF -KB signaling activation decrease the colonization of E. piscicida and rescue the mortality of larvae. Taken together, our study reveals that TLR5b-mediated NF -KB activation promotes cxcl8a-dependent neutrophils recruitment to defense E. piscicida infection in zebrafish, which contributes to better understanding the mechanism of NF -KB signaling activation in teleost fish.
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页数:8
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