Vibrio harveyi causes vibriosis in nearly 70% of grouper (Epinephelus sp.), seriously limiting grouper culture. As well as directly inhibiting pathogens, the gut microbiota plays critical roles in immune homeostasis and provides essential health benefits to its host. However, there is still little information about the variations in the immune response to V. harveyi infection and the gut microbiota of grouper. To understand the virulence mechanism of V. harveyi in the pearl gentian grouper, we investigated the variations in the pathological changes, immune responses, and gut bacterial communities of pearl gentian grouper after exposure to differently virulent V. harveyi strains. Obvious histopathological changes were detected in heart, kidney, and liver. In particular, nodules appeared and huge numbers of V. harveyi cells colonized the liver at 12 h postinfection (hpi) with highly virulent V. harveyi. Although no V. harveyi was detected in the gut, the infection simultaneously induced a gut-liver immune response. In particular, the expression of 8 genes associated with cellular immune processes, including genes encoding inflammatory cytokines and receptors, and pattern recognition proteins, was markedly induced by V. harveyi infection, especially with the highly virulent V. harveyi strain. V. harveyi infection also induced significant changes in gut bacterial community, in which Vibrio and Photobacterium increased but Bradyrhizobium, Lactobacillus, Blautia, and Faecalibaculum decreased in the group infected with the highly virulent strain, with accounting for 82.01% dissimilarity. Correspondingly, four bacterial functions related to bacterial pathogenesis were increased by infection with highly virulent V. harveyi, whereas functions involving metabolism and genetic information processing were reduced. These findings indicate that V. harveyi colonizes the liver and induces a gut-liver immune response that substantially disrupts the composition of and interspecies interactions in the bacterial community in fish gut, thereby altering the gut-microbiota-mediated functions and inducing fish death.

哈维弧菌 导致将近70％的石斑鱼发生弧菌病（石斑鱼sp。），严重限制了石斑鱼文化。除直接抑制病原体外，肠道菌群在免疫稳态中也起着关键作用，并为其宿主提供基本的健康益处。但是，关于针对小鼠的免疫应答变化的信息仍然很少。哈维感染和石斑鱼的肠道菌群。了解毒力的机制哈维 在珍珠龙胆石斑鱼中，我们调查了不同毒性的珍珠龙胆石斑鱼的病理变化，免疫反应和肠道细菌群落的变化 哈维株。在心脏，肾脏和肝脏中检测到明显的组织病理学变化。特别是出现结节，大量结节哈维 细胞在感染后12 h（hpi）进入肝细胞，并具有高毒性 哈维（V. harveyi）。 虽然没有 哈维在肠道中检测到这种感染，该感染同时诱导了肠肝免疫反应。特别是，与细胞免疫过程有关的8个基因的表达，包括编码炎性细胞因子和受体的基因以及模式识别蛋白，被下列基因显着诱导。哈维 感染，尤其是剧毒 哈维 应变。 哈维 感染还引起肠道细菌群落的显着变化，其中 弧菌 和 光细菌 增加但 缓生根瘤菌， 乳杆菌， 布劳蒂亚和 粪杆菌高毒力菌株感染组的病毒感染率下降，占相异性的82.01％。相应地，高致病性感染增加了与细菌发病相关的四种细菌功能哈维，而涉及代谢和遗传信息处理的功能则减少了。这些发现表明哈维 在肠道中定居，并诱导肠道-肝脏免疫反应，从而实质上破坏鱼肠细菌群落的组成和种间相互作用，从而改变肠菌群介导的功能并导致鱼死亡。