文献类型： 外文期刊
作者： Gao, Fengying 1 ; Pang, Jicai 3 ; Lu, Maixin 1 ; Liu, Zhigang 1 ; Wang, Miao 1 ; Ke, Xiaoli 1 ; Yi, Mengmeng 1 ; Cao, Jianmeng 1 ;
作者机构： 1.Chinese Acad Fishery Sci, Pearl River Fisheries Res Inst, Key Lab Trop & Subtrop Fishery Resource Applicat &, Minist Agr, Guangzhou 510380, Peoples R China
2.Chinese Acad Fishery Sci, Pearl River Fisheries Res Inst, Guangdong Prov Key Lab Aquat Anim Immune Technol, Guangzhou 510380, Peoples R China
3.Shandong Vocat Anim Sci & Vet Coll, Weifang 261021, Shandong, Peoples R China
4.Chinese Acad Fishery Sci, Pearl River Fisheries Res Inst, 1 Xing Yu Rd, Guangzhou 510380, Guangdong, Peoples R China
关键词： Nile tilapia ( Oreochromis niloticus ); TLR5; Immune response; NF-KB activation; Coimmunoprecipitation; Flagellin
期刊名称：DEVELOPMENTAL AND COMPARATIVE IMMUNOLOGY （ 影响因子：3.605； 五年影响因子：3.833 ）
ISSN： 0145-305X
年卷期： 2022 年 133 卷
页码：
收录情况： SCI
摘要： Toll-like receptor 5 (TLR5) is responsible for bacterial flagellin recognition in vertebrates. In the present study, TLR5M was identified in the Nile tilapia Oreochromis niloticus (OnTLR5), containing a conserved LRR domain, a transmembrane region and a C-terminal TIR domain, similar to that of other fishes and mammals. OnTLR5 was broadly expressed in all the tissues examined, presenting the highest expression levels in the blood and the lowest in the kidney. OnTLR5 was detected from 2 d postfertilization (dpf) to 8 dpf during embryonic development. Moreover, expression levels of OnTLR5 were clearly altered in all five tissues examined in response to Streptococcus agalactiae infection in vivo. Overexpression of OnTLR5 in HEK293T cells revealed that OnTLR5 was distributed in the cytoplasm and significantly increased NF-KB activation. In response to cotransfection with OnMyd88, OnTLR5 significantly upregulated OnMyd88-induced NF-KB activation. Pulldown assays showed that OnTLR5 interacts with OnMyd88 and revealed an interaction between TLR5 and Aeromonas hydrophila flagellin. Taken together, these findings suggest that OnTLR5 plays important roles in TLR/IL-1R signalling pathways and the immune response to pathogen invasion.
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