Abstract：
The mechanism by which Y. ruckeri infection induces enteritis in Chinese sturgeon remains unclear, and the efficacy of drug prevention and control measures is not only poor but also plagued with numerous issues. We conducted transcriptomic and 16 S rRNA sequencing analyses to examine the differences in the intestinal tract of hybrid sturgeon before and after Y. ruckeri infection and florfenicol intervention. Our findings revealed that Y. ruckeri induced the expression of multiple inflammatory factors, including il1β, il6, and various chemokines, as well as casp3, casp8, and multiple tumor necrosis factor family members, resulting in pathological injury to the body. Additionally, at the phylum level, the relative abundance of Firmicutes and Bacteroidota increased, while the abundance of Plesiomonas and Cetobacterium decreased at the genus level, altering the composition of the intestinal flora. Following florfenicol intervention, the expression of multiple apoptosis and inflammation-related genes was down-regulated, promoting tissue repair. However, the flora became further dysregulated, increasing the risk of infection. In conclusion, our analysis of the transcriptome and intestinal microbial composition demonstrated that Y. ruckeri induces intestinal pathological damage by triggering apoptosis and altering the composition of the intestinal microbiota. Florfenicol intervention can repair pathological damage, but it also exacerbates flora imbalance, leading to a higher risk of infection. These findings help elucidate the molecular mechanism of Y. ruckeri-induced enteritis in sturgeon and evaluate the therapeutic effect of drugs on intestinal inflammation in sturgeon.
摘要：
牛肝菌感染引起中华民国肠炎的机制尚不清楚，药物预防和控制措施不仅效果不佳，而且还困扰着许多问题。我们进行了转录组学和16SrRNA测序分析，以检查Y.ruckeri感染和氟苯尼考干预前后杂种st的肠道差异。我们的发现表明Y.ruckeri诱导多种炎症因子的表达，包括IL1β，il6和各种趋化因子，以及casp3，casp8和多个肿瘤坏死因子家族成员，对身体造成病理性伤害。此外,在门的水平，Firmicutes和拟杆菌的相对丰度增加，而在属水平上，泛单胞菌属和环菌属的丰度下降，改变肠道菌群的组成。氟苯尼考干预后，多个细胞凋亡和炎症相关基因表达下调,促进组织修复。然而,植物区系进一步失调，增加感染的风险。总之,我们对转录组和肠道微生物组成的分析表明，Y.ruckeri通过触发细胞凋亡和改变肠道微生物组成来诱导肠道病理损伤。氟苯尼考干预可修复病理损伤，但它也加剧了菌群失衡，导致更高的感染风险。这些发现有助于阐明Y.ruckeri引起的st鱼肠炎的分子机制，并评估药物对st鱼肠道炎症的治疗作用。
