Jia Longwu, Zhang Lele, Yang Hongwei, Li Lin, Zheng Shiyi, Ma Yicong, Xue Yuanyuan, Zhang Jingyi, Li Mingzhu, Su Xiaolei, Wang Kai
School of Fisheries, Ludong University, Yantai, 264025, China; Research and Development Center of Science, Technology and Industrialization of Seahorses, Ludong University, Yantai, 264025, China.
School of Fisheries, Ludong University, Yantai, 264025, China; Research and Development Center of Science, Technology and Industrialization of Seahorses, Ludong University, Yantai, 264025, China.
Fish Shellfish Immunol. 2025 Jan;156:110024. doi: 10.1016/j.fsi.2024.110024. Epub 2024 Nov 16.
Edwardsiella piscicida-induced lethal enteritis is a major threat to the sustainable development of seahorse aquaculture. The roles of Carbohydrate-Active enzymes (CAZymes) in interactions between the pathogen and the host are poorly understood. In this study, we found that 22 key CAZymes encoded by E. piscicida might involve in the coordination of five key stages of infection. Specifically, during the motility, adherence, and invasion stages, 10 CAZymes, including CE4, PL8, and CBM48, may significantly increase the activities of Lipid metabolism-associated pathways of the intestinal microbiota (P < 0.01), facilitating pathogen invasion of the host intestinal epithelium. During the replication stage, 11 CAZymes, including GH20, GT4, and GH3, may significantly increase activities of pathways associated with Carbohydrate metabolism (P < 0.01) to promote replication and proliferation of the pathogen. And for avoiding host defenses, GH2 and GH1 may enhance activities of both Carbohydrate and Amino acid metabolic pathways (P < 0.01), facilitating infection and immune evasion. Conjoint analysis showed that E. piscicida might mainly rely on Carbohydrate metabolism for infection, while the host might activate Amino acid metabolic pathways for self-defense. In addition, expressions of 10 key genes, Aldh9a1b, Aoc1, Tpi1b, PCK1, Ldha, Me1, Gla, Cel.2, Ugdh, and Mao, were significantly altered (P < 0.01) and may be used for characterizing host responses to E. piscicida infection. Activities of both Glycolysis/Gluconeogenesis and Tryptophan metabolism were found oppositely changed (P < 0.01) between pathogen and host, respectively, representing the primary focuses of the competition. Overall, this study provides new insights into E. piscicida-mediated intestinal enteritis in fish for the first time from the perspective of CAZymes, as well as a theoretical reference for the prevention and control of these diseases in the aquaculture of seahorses and other fish.
杀鱼爱德华氏菌引起的致死性肠炎是海马养殖业可持续发展的主要威胁。人们对碳水化合物活性酶（CAZymes）在病原体与宿主相互作用中的作用了解甚少。在本研究中，我们发现杀鱼爱德华氏菌编码的22种关键CAZymes可能参与感染五个关键阶段的协调。具体而言，在运动、黏附和侵入阶段，包括CE4、PL8和CBM48在内的10种CAZymes可能会显著增加肠道微生物群脂质代谢相关途径的活性（P<0.01），促进病原体对宿主肠上皮的侵入。在复制阶段，包括GH20、GT4和GH3在内的11种CAZymes可能会显著增加与碳水化合物代谢相关途径的活性（P<0.01），以促进病原体的复制和增殖。为了逃避宿主防御，GH2和GH1可能会增强碳水化合物和氨基酸代谢途径的活性（P<0.01），促进感染和免疫逃逸。联合分析表明，杀鱼爱德华氏菌可能主要依靠碳水化合物代谢进行感染，而宿主可能会激活氨基酸代谢途径进行自我防御。此外，10个关键基因Aldh9a1b、Aoc1、Tpi1b、PCK1、Ldha、Me1、Gla、Cel.2、Ugdh和Mao的表达发生了显著变化（P<0.01），可用于表征宿主对杀鱼爱德华氏菌感染的反应。分别在病原体和宿主之间发现糖酵解/糖异生和色氨酸代谢的活性发生了相反的变化（P<0.01），这代表了竞争的主要焦点。总体而言，本研究首次从CAZymes的角度为杀鱼爱德华氏菌介导的鱼类肠道肠炎提供了新见解，也为海马和其他鱼类养殖中这些疾病的防控提供了理论参考。
