Clock gene NR1D1 mediated inflammatory response after Streptococcus agalactiae challenge in Nile Tilapia (Oreochromis niloticus) brain
文献类型： 外文期刊
作者： Wang, Zhang 1 ; Liu, Zhigang 1 ; Zhu, Weijuan 1 ; Zhang, Meiyan 1 ; Huang, Shaowei 1 ; Cao, Jianmeng 1 ; Wang, Miao 1 ; Yi, Mengmeng 1 ; Gao, Fengying 1 ; Lu, Maixin 1 ; Ke, Xiaoli 1 ;
作者机构： 1.Chinese Acad Fisheries Sci, Pearl River Fisheries Res Inst, Key Lab Trop & Subtrop Fishery Resource Applicat &, Minist Agr, Guangzhou 510380, Peoples R China
2.Shanghai Ocean Univ, Coll Fisheries & Life Sci, Shanghai 201306, Peoples R China
关键词： S. agalactiae; Neuronal injury; NF-kappa B; Astrocytes inflammatory response
期刊名称：AQUACULTURE REPORTS （ 影响因子：3.7； 五年影响因子：4.0 ）
ISSN： 2352-5134
年卷期： 2025 年 43 卷
页码：
收录情况： SCI
摘要： Neuronal injury caused by Streptococcus agalactiae (S. agalactiae) poses a threat to the survival of tilapia. However, the molecular regulatory mechanisms underlying this process remain largely unknown. In this study, a comparative transcriptome analysis suggested that the biological rhythm pathway and the rhythm gene NR1D1 may be responsible for defending against S. agalactiae infection in tilapia brains. Bioinformatics-based methods revealed that NR1D1 shared high similarity in domains with its vertebrate homologs. A spatio-temporal expression analysis showed that NR1D1 was highly expressed in the blood, gill, intestinal, heart, brain, and muscle of healthy tilapia. S. agalactiae infection disrupted the oscillatory expression patterns of NR1D1 and induced its expression in the tilapia brain. A dual-luciferase reporter assay found that NR1D1 suppressed the NF kappa B pathway in both normal and S. agalactiae-infected astrocytes of tilapia. The NF-kappa B agonist diprovocim alleviated the decrease in cell viability and mitigated astrocyte apoptosis induced by NR1D1 overexpression (via pNR1D1 treatment) after S. agalactiae infection. Moreover, the expression of pro-inflammatory markers (TNF-alpha, IL-6 and IL-1 beta) was reduced in association with NR1D1 overexpression, and this repression could be partially rescued by co-treatment with pNR1D1 and diprovocim in astrocytes. However, the mRNA levels of the antiinflammatory gene IL-10 were upregulated by either pNR1D1 or diprovocim treatment. Altogether, this study provide new insights into the pathogenic mechanism of NR1D1 in tilapia brain following S. agalactiae infection.
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