在Siluriformes中感染拟态弧菌已显示出快速且高的传染性和死亡率,与其他主机不同。我们之前的调查发现坏死,一场煽动性的风暴,和组织重塑是感染V.mimicus的黄cat鱼(Pelteobagrusfulvidraco)的关键病理反应。这项研究的目的是进一步阐明在模仿弧菌感染期间将宿主内的这些病理反应联系起来的影响。使用代谢组学和转录组学,我们发现了感染诱导的膜周密集空泡化;与核苷酶和肽酶活性相关的几个基因在受感染鱼的皮肤和肌肉中显著上调。同时,宿主细胞的翻译过程受损。进一步的调查表明,拟态弧菌通过增强其新陈代谢来完成其感染过程,包括利用寡肽和核苷酸。黄cat鱼对拟态弧菌感染的高度敏感性与其体表组成有关,它提供了富含各种核苷酸的微环境,如dIMP,dAMP,脱氧鸟苷,和ADP,除了几个氨基酸和肽。这些代谢物中的一些显着促进拟态弧菌的生长和运动,从而影响其生物学功能。此外,我们发现黄鲶鱼表面神经节苷脂的表达升高,帮助拟态弧菌粘连并增加其感染风险。值得注意的是,我们观察到黄鲶鱼的皮肤和肌肉缺乏超过25种多不饱和脂肪酸,比如二十碳五烯酸,12-氧代-ETE,和13-Oxo-ODE。这些物质在抗炎机制中发挥作用,可能导致在黄鲶鱼中观察到的免疫失调。总之,我们的研究揭示了宿主免疫偏差现象,通过增加营养供应促进细菌定植。它强调了使黄cat鱼高度易感V.mimicus的关键因素,表明宿主营养来源不仅能够在宿主内建立和维持感染,而且还有助于细菌在免疫压力下生存,最终完成其生命周期。
Infection with Vibrio mimicus in the Siluriformes has demonstrated a rapid and high infectivity and mortality rate, distinct from other hosts. Our earlier investigations identified necrosis, an inflammatory storm, and tissue remodeling as crucial pathological responses in yellow catfish (Pelteobagrus fulvidraco) infected with V. mimicus. The objective of this study was to further elucidate the impact linking these pathological responses within the host during V. mimicus infection. Employing metabolomics and transcriptomics, we uncovered infection-induced dense vacuolization of perimysium; Several genes related to nucleosidase and peptidase activities were significantly upregulated in the skin and muscles of infected fish. Concurrently, the translation processes of host cells were impaired. Further investigation revealed that V. mimicus completes its infection process by enhancing its metabolism, including the utilization of oligopeptides and nucleotides. The high susceptibility of yellow catfish to V. mimicus infection was associated with the composition of its body surface, which provided a microenvironment rich in various nucleotides such as dIMP, dAMP, deoxyguanosine, and ADP, in addition to several amino acids and peptides. Some of these metabolites significantly boost V. mimicus growth and motility, thus influencing its biological functions. Furthermore, we uncovered an elevated expression of gangliosides on the surface of yellow catfish, aiding V. mimicus adhesion and increasing its infection risk. Notably, we observed that the skin and muscles of yellow catfish were deficient in over 25 polyunsaturated fatty acids, such as Eicosapentaenoic acid, 12-oxo-ETE, and 13-Oxo-ODE. These substances play a role in anti-inflammatory mechanisms, possibly contributing to the immune dysregulation observed in yellow catfish. In summary, our study reveals a host immune deviation phenomenon that promotes bacterial colonization by increasing nutrient supply. It underscores the crucial factors rendering yellow catfish highly susceptible to V. mimicus, indicating that host nutritional sources not only enable the establishment and maintenance of infection within the host but also aid bacterial survival under immune pressure, ultimately completing its lifecycle.