Abstract：
Bacterial intestinal inflammation is a common disease of yellow catfish (Pelteobagrus fulvidraco) in high-density aquaculture. Understanding the interactions between host and intestinal bacteria is helpful to intestinal inflammatory disease control. Here, we constructed a model of intestinal inflammation after Aeromonas hydrophila infection in yellow catfish, and characterized variations in gene expression and microbiome in the gut through high-throughput sequencing. Furthermore, host gene-microbiome interactions were identified. Histology observation showed disordered distribution of columnar epithelial cells and decrease of goblet cells in intestine. A total of 4741 genes showed differentially expression, mostly in comparisons between 12 hpi group with each other groups respectively, including control, 24 hpi and 48 hpi groups. These genes were enriched in immune-related pathways including the IL-17 signaling pathway, triggering strong inflammatory response at the invading stage within 12 h. Subsequently, the host strengthened energy consumption by activating carbohydrate and lipid metabolism pathways to repair the intestinal mucosal immune defense line. In addition, fish with A. hydrophila infection show decreased richness of gut microbial, reduced relative abundance of probiotics including Akkermansia, and elevated pathogenic bacteria such as Plesimonas. An integrative analysis identified A. hydrophila-related genes, such as il22 and stat3, for which expression level is close associated with the shift of A. hydrophila-related bacteria relative abundance, such as Akkermansia and Cetobacterium. Aside from picturing the variations of intestine gene expression and mucosal microbiome of yellow catfish coping with A. hydrophila infection, our study probed the underlying host-microbe interactions in A. hydrophila infection induced intestinal inflammatory, providing new insights for disease control in aquaculture.
摘要：
细菌性肠道炎症是黄of鱼（Pelteobagrusfulvidraco）在高密度水产养殖中的常见疾病。了解宿主与肠道细菌之间的相互作用有助于肠道炎性疾病的控制。这里,我们构建了黄鲶鱼嗜水气单胞菌感染后肠道炎症模型，并通过高通量测序表征肠道中基因表达和微生物组的变化。此外，确定了宿主基因-微生物组相互作用。组织学观察显示，肠道柱状上皮细胞分布紊乱，杯状细胞减少。共有4741个基因显示差异表达，主要是在12个hpi组分别与其他组之间进行比较，包括控制，24hpi和48hpi组。这些基因富含免疫相关途径，包括IL-17信号通路，在12小时内，在入侵阶段引发强烈的炎症反应。随后，宿主通过激活碳水化合物和脂质代谢途径来增强能量消耗，以修复肠黏膜免疫防线。此外,感染嗜水菌的鱼显示肠道微生物的丰富度降低，降低益生菌的相对丰度，包括Akkermansia，和升高的致病菌，如Plesimonas。综合分析确定了嗜水气单胞菌相关基因，如il22和stat3，其表达水平与嗜水气单胞菌相关细菌相对丰度的变化相关，如Akkermansia和Cetobacterium。除了描绘应对嗜水菌感染的黄鲶鱼的肠道基因表达和粘膜微生物组的变化外，我们的研究探讨了嗜水气单胞菌感染引起的肠道炎症中潜在的宿主-微生物相互作用，为水产养殖疾病控制提供新的见解。
