Liao Minze, Liao Xuzheng, Long Xinxin, Zhao Jichen, He Zihao, Zhang Jingyue, Wu Tingfen, Sun Chengbo
College of Fisheries, Guangdong Ocean University, Zhanjiang, Guangdong, China.
School of Marine Sciences, Sun Yat-sen University, Guangzhou, China.
Front Microbiol. 2023 Jan 13;13:1097931. doi: 10.3389/fmicb.2022.1097931. eCollection 2022.
Decapod iridescent virus 1 (DIV1) has caused severe economic losses in shrimp aquaculture. So far, Researchs on DIV1-infected shrimp have mainly focused on the hemocytes immune response, while studies on the host-intestine microbiota interactions during DIV1 infection have been scarce.
This study determined the lethal concentration 50 (LC) of DIV1 to , preliminarily determining that could serve as a susceptible object for DIV1. The interactions and responses between the immune and intestine microbiota of shrimp under DIV1 infection were also investigated.
DIV1 infection decreases intestine bacterial diversity and alters the composition of intestine microbiota. Specifically, DIV1 infection decreases the abundance of potentially beneficial bacteria (Bacteroidetes, Firmicutes, and Actinobacteria), and significantly increases the abundance of pathogenic bacteria such as and , thereby increasing the risk of secondary bacterial infections. The results of PICRUSt functional prediction showed that altered intestine microbiota induces host metabolism disorders, which could be attributed to the bioenergetic and biosynthetic requirements for DIV1 replication in shrimp. The comparative transcriptomic analysis showed that some metabolic pathways related to host immunity were significantly activated following DIV1 infection, including ncRNA processing and metabolic process, Ascorbate and aldarate metabolism, and Arachidonic acid metabolism. may against DIV1 infection by enhancing the expression of some immune-related genes, such as Wnt16, heat shock protein 90 (Hsp90) and C-type lectin 3 (Ctl3). Notably, correlation analysis of intestinal microbial variation with host immunity showed that expansion of pathogenic bacteria ( and ) in DIV1 infection could increased the expression of NF-κB inhibitors cactus-like and Toll interacting protein (Tollip), which may limit the TLR-mediated immune response and ultimately lead to further DIV1 infection.
This study enhances our understanding of the interactions between shrimp immunity and intestinal microbiota. The ultimate goal is to develop novel immune enhancers for shrimp and formulate a safe and effective DIV1 defense strategy.
十足目虹彩病毒1(DIV1)已给对虾养殖业造成严重经济损失。到目前为止,关于DIV1感染对虾的研究主要集中在血细胞免疫反应上,而对于DIV1感染期间宿主肠道微生物群相互作用的研究却很少。
本研究测定了DIV1对[具体物种]的半数致死浓度(LC),初步确定[具体物种]可作为DIV1的易感对象。同时还研究了DIV1感染下对虾免疫与肠道微生物群之间的相互作用和反应。
DIV1感染会降低肠道细菌多样性并改变肠道微生物群的组成。具体而言,DIV1感染会降低潜在有益细菌(拟杆菌门、厚壁菌门和放线菌门)的丰度,并显著增加[具体病原菌1]和[具体病原菌2]等病原菌的丰度,从而增加继发细菌感染的风险。PICRUSt功能预测结果表明,肠道微生物群的改变会引发宿主代谢紊乱,这可能归因于DIV1在对虾体内复制所需的生物能量和生物合成需求。比较转录组分析表明,DIV1感染后,一些与宿主免疫相关的代谢途径被显著激活,包括非编码RNA加工和代谢过程、抗坏血酸和醛糖代谢以及花生四烯酸代谢。[具体物质]可能通过增强一些免疫相关基因(如Wnt16、热休克蛋白90(Hsp90)和C型凝集素3(Ctl3))的表达来抵抗DIV1感染。值得注意的是,肠道微生物变化与宿主免疫的相关性分析表明,DIV1感染中病原菌([具体病原菌1]和[具体病原菌2])的扩增会增加NF-κB抑制剂类仙人掌蛋白和Toll相互作用蛋白(Tollip)的表达,这可能会限制TLR介导的免疫反应,并最终导致DIV1进一步感染。
本研究增进了我们对虾免疫与肠道微生物群之间相互作用的理解。最终目标是开发新型对虾免疫增强剂,并制定安全有效的DIV1防御策略。