High nutrient induces virulence in the AHPND-causing Vibrio parahaemolyticus, interpretation from the ecological assembly of shrimp gut microbiota
High nutrient induces virulence in the AHPND-causing Vibrio parahaemolyticus, interpretation from the ecological assembly of shrimp gut microbiota
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高营养诱导引起 AHPND 的副溶血弧菌的毒力，从虾肠道微生物群的生态组装解释
DOI：
10.1016/j.fsi.2022.07.016
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发表时间：
2022
影响因子：
4.7
通讯作者：
Jinbo Xiong
中科院分区：
文献类型：
--
作者：
Haonan Sha;Luyue Li;Jiaqi Lu;Jinbo Xiong
对虾病害多发生在养殖后期，此时养殖水体已富营养化。这一观察结果提示，病原体的毒力可能是由营养升高引起的，而潜在的生态机制仍然有限。为了解决这一紧迫的知识，我们探索了肠道微生物群如何对低营养（OVp）或富营养（EVp）预培养的副溶血性弧菌（虾急性肝胰腺坏死病（AHPND）的一种致病病原体）的感染作出反应。结果表明，OVp和EVp感染引起肠道菌群失调，导致对虾免疫功能低下，感染越晚，死亡率越早，死亡率越高。在肠道微生物群和每一种测量的免疫活性之间检测到显著的关联。中性群落模型表明，EVp感染后，肠道菌群的聚集受确定性过程的支配更强，其次是EVp感染虾和对照虾。此外，EVp感染对虾肠道菌群的时间周转率和平均变异程度显著低于对照组。值得注意的是，在排除了个体效应后，我们确定了22个感染歧视分类群。以22个指标的剖面图作为自变量，诊断模型准确区分感染状态（对照、OVp或EVp感染虾），总体准确率为85.9%，在感染初期准确率为81.3%。EVp感染对虾肠道菌群的趋同性和确定性可以从生态学角度部分解释为什么APHND的治疗具有挑战性。此外，我们提供了一种敏感的方法来诊断感染的开始，当疾病症状是不可观察的。•EVp感染导致肠道菌群快速失调，导致虾的死亡率更高。•肠道菌群的组装更强烈地受到EVp感染的确定性过程的控制。•EVp感染的虾降低了肠道微生物群的周转率和平均变异程度。•诊断模型准确识别感染状态（准确率85.9%）。
Shrimp diseases frequently occur during the later farming stages, when the rearing water is eutrophic. This observation provides clue that the virulence of pathogens could be induced by elevated nutrient, whereas the underlying ecological mechanism remains limited. To address this pressing knowledge, we explored how gut microbiota responded to the infection of oligotrophic (OVp) or eutrophic (EVp) pre-cultured Vibrio parahaemolyticus , a causing pathogen of shrimp acute hepatopancreatic necrosis disease (AHPND). Resulted revealed that OVp and EVp infections caused dysbiosis in the gut microbiota and compromised shrimp immunity, while the later infection led to earlier and higher mortality. Significant associations were detected between the gut microbiota and each of the measured immune activities. Neutral community model showed that the assembly of gut microbiota was more strongly governed by deterministic processes in EVp infection, followed by EVp infected and control shrimp. Additionally, there were significantly lower temporal turnover rate and average variation degree in the gut microbiota in EVp infected shrimp compared with control individuals. Notably, we identified 22 infection-discriminatory taxa after ruling out the ontogenic effect. Using profiles of the 22 indicators as independent variables, the diagnosis model accurately distinguished (an overall 85.9% accuracy) the infected status (control, OVp or EVp infected shrimp), with 81.3% accuracy at the initial infection stage. The convergent and deterministic gut microbiota in EVp infected shrimp could partially explain why it is challenge to cure APHND from an ecological viewpoint. In addition, we provided a sensitive approach for diagnosing the onset of infection, when disease symptom is unobservable. • EVp infection causes rapid dysbiosis in the gut microbiota, leads to earlier and higher shrimp mortality. • The assembly of gut microbiota is more strongly governed by deterministic processes in EVp infection. • EVp infected shrimp decreases turnover rate and average variation degree in the gut microbiota. • Diagnosis model accurately distinguishes (85.9% accuracy) the infected status.