Edwardsiella piscicida (E. piscicida) is an important zoonotic pathogen that mostly infects fish by colonizing the intestine. Fucose within the intestine could regulate the pathogenicity of some intestinal pathogens. Here we identified the function of fucose permease in E. piscicida and its physiological influence. The results showed that E. piscicida grew faster in the presence of l-fucose. The fucose permease gene fucP mutant strain ΔfucP significantly decreased penetration and motility in mucin compared with the wild-type strain. The gene expression levels of esaB, esaD, esaL and esaK in ΔfucP had significantly downregulated when compared with the wild-type strain. Most importantly, the survival rate of zebrafish after being infected with ΔfucP was significantly higher than those of the wild type. In a word, fucose promoted the growth and motility of E. piscicida and the fucP gene mutant decreased the pathogenicity of E. piscicida in zebrafish.

爱德华氏菌（E. piscicida）是一种重要的人畜共患病原体，主要通过在肠道内定殖来感染鱼类。肠道内的岩藻糖可以调节某些肠道病原体的致病性。在这里，我们确定了岩藻通透酶在E. piscicida中的功能及其生理影响。结果表明，E. piscicida增长中存在快升岩藻糖。与野生型菌株相比，岩藻糖渗透酶基因fuc P突变株Δfuc P显着降低了粘蛋白的渗透性和运动性。的基因表达水平ESA B，ESA d，ESA L和与野生型菌株相比，Δfuc P中的esa K显着下调。最重要的是，斑马鱼被Δfuc P感染后的存活率显着高于野生型。简而言之，岩藻糖促进了大肠杆菌的生长和运动，而fuc P基因突变体降低了斑马鱼中大肠杆菌的致病性。