作者
Yuanbo Li,Yuanbo Li,Yuanbo Li,Jiabao Hu,Jiabao Hu,Jiabao Hu,Jiabao Hu,Youyi Zhang,Youyi Zhang,Youyi Zhang,Kaiheng Yan,Kaiheng Yan,Kaiheng Yan,Xubo Wang,Xubo Wang,Xubo Wang,Suming Zhou,Suming Zhou,Suming Zhou,Shanliang Xu,Shanliang Xu,Shanliang Xu,Xiaojun Yan,Xiaojun Yan,Xiaojun Yan,Yajun Wang,Yajun Wang,Yajun Wang
摘要
The complement system is pivotal in innate immune defense, with Complement 1qb (C1qb) playing a key role in recognizing immune complexes and initiating the classical pathway. In this research, we cloned the full-length cDNA of silver pomfret (Pampus argenteus) c1qb and demonstrated its role in mediating defense responses against Nocardia seriolae (N. seriolae) infection, which notably causes significant economic losses in the aquaculture industry. Our investigation revealed that N. seriolae infection led to tissue damage in fish bodies, as observed in tissue sections. Subsequent analysis of differential genes (DEGs) in the transcriptome highlighted genes linked to apoptosis and inflammation. Through experiments involving overexpression and interference of c1qb in vitro, we confirmed that c1qb could suppress N. seriolae-induced apoptosis and inflammation. Moreover, overexpression of c1qb hindered N. seriolae invasion, and the purified and replicated C1qb protein displayed antimicrobial properties. Additionally, our study unveiled that overexpression of c1qb might stimulate the expression of membrane attack complexes (MAC), potentially enhancing opsonization and antibacterial effects. In conclusion, our findings offer valuable insights into the immune antibacterial mechanisms of c1qb and contribute to the development of strategies for controlling N. seriolae.