Duan Yafei, Huang Jianhua, Wang Yun, Yang Yukai, Li Hua
State Key Laboratory of Mariculture Biobreeding and Sustainable Goods, Key Laboratory of South China Sea Fishery Resources Exploitation & Utilization, Ministry of Agriculture and Rural Affairs, South China Sea Fisheries Research Institute, Chinese Academy of Fishery Sciences, Guangzhou, 510300, PR China; Key Laboratory of Efficient Utilization and Processing of Marine Fishery Resources of Hainan Province, Sanya Tropical Fisheries Research Institute, Sanya, 572018, PR China.
Shenzhen Base of South China Sea Fisheries Research Institute, Chinese Academy of Fishery Sciences, Shenzhen, 518121, PR China.
Fish Shellfish Immunol. 2025 Sep 2;167:110701. doi: 10.1016/j.fsi.2025.110701.
High-temperature (HT) is a critical influencing factor in shrimp aquaculture and serves as a key trigger for frequent disease outbreaks in shrimp. As a core organ for digestion, absorption and immune defense, the intestine's functional homeostasis is the key foundation for shrimp health. Therefore, in this study, the shrimp Litopenaeus vannamei were continuously exposed to HT stress at 33 °C for 7 days, after which the changes in intestinal functional homeostasis were investigated based on the mucosal integrity, immune signaling, and microbial community. The results showed that HT stress caused intestinal epithelial detachment and mucosal damage, as well as the disruption of the mucus barrier, including the upregulation of MUC2, MUC3A and MUC3B genes and the downregulation of MUC1 and MUC4 genes. Additionally, oxidative stress-related genes, such as the expressions of ROMO1, Nrf2, GPx and HO1 were upregulated, while the expression of SOD was downregulated; antimicrobial genes, such as the expressions of Crus and proPO were upregulated, whereas the expressions of ALF, Pen3 and Lys were downregulated; inflammatory genes (JNK and NF-κB) and autophagy genes (Atg3, Atg12, Beclin1 and Hsc70) expression were all upregulated. In terms of intestinal microbiota, microbial diversity showed no significant changes, but the abundance of community composition was perturbed, particularly the homeostasis of putative harmful bacteria (Vibrio and Photobacterium) and beneficial bacteria (Bacteroides, Bacillus, Lactobacillus, and Lactococcus). Additionally, the phosphotransferase system (PTS) function of the intestinal microbiota was enhanced, while the functions such as N-glycan biosynthesis and glycosaminoglycan degradation were weakened. These results demonstrated that HT stress disrupted intestinal functional homeostasis by inducing mucosal damage, disrupting the mucus barrier and immune responses, activating oxidative stress, inflammation, and autophagy signaling, and reshaping the microbial community.
高温（HT）是对虾养殖中的一个关键影响因素，也是对虾频繁爆发疾病的关键诱因。作为消化、吸收和免疫防御的核心器官，肠道功能的稳态是对虾健康的关键基础。因此，在本研究中，凡纳滨对虾持续暴露于33°C的高温胁迫7天，之后基于黏膜完整性、免疫信号和微生物群落研究肠道功能稳态的变化。结果表明，高温胁迫导致肠道上皮脱落和黏膜损伤，以及黏液屏障的破坏，包括MUC2、MUC3A和MUC3B基因上调，而MUC1和MUC4基因下调。此外，氧化应激相关基因，如ROMO1、Nrf2、GPx和HO1的表达上调，而SOD的表达下调；抗菌基因，如Crus和proPO的表达上调，而ALF、Pen3和Lys的表达下调；炎症基因（JNK和NF-κB）和自噬基因（Atg3、Atg12、Beclin1和Hsc70）的表达均上调。在肠道微生物群方面，微生物多样性无显著变化，但群落组成的丰度受到干扰，特别是假定有害细菌（弧菌属和发光杆菌属）和有益细菌（拟杆菌属、芽孢杆菌属、乳杆菌属和乳球菌属）的稳态。此外，肠道微生物群的磷酸转移酶系统（PTS）功能增强，而N-聚糖生物合成和糖胺聚糖降解等功能减弱。这些结果表明，高温胁迫通过诱导黏膜损伤、破坏黏液屏障和免疫反应、激活氧化应激、炎症和自噬信号以及重塑微生物群落来破坏肠道功能稳态。
