UhpA in Edwardsiella piscicida decreases the pathogenicity and the capability of inducing cytokine response in zebrafish

Abstract

Edwardsiella piscicida (E. piscicida) is one of the main pathogens of fish, which could invade the host through the gut. Glucose 6-phosphate (Glu6P) within the gut provides environmental stresses that affect the pathogenicity of bacteria. Here we focus on a novel two-component chemical signal transduction system, named UhpB/UhpA in E. piscicida, including the key component hexose phosphate transport system regulatory protein (UhpA) coded by the uhpA gene. This study will elucidate the functions of the uhpA gene in the pathogenicity of E. piscicida and the immune response in zebrafish when infected with E. piscicida. The results showed that the wild type strain of E. piscicida EIB202 demonstrated significant increases in growth compared to the mutant strain ΔuhpA with or without 20 mM Glu6P (P < 0.05). The LD50 of E. piscicida △uhpA strain (2 × 104 CFU/fish) for zebrafish was significantly lower than the wild-type strain (1 × 105 CFU/fish), which suggested the uhpA gene deletion could increase its virulence. Besides, fish infected with ΔuhpA showed significantly higher (p < 0.05) gene expression of IL-1β and TGF-β in spleen than fish infected with EIB202 at 6 h, 12 h, 24 h, and 48 h after infection, TNF-α in spleen of fish infected with ΔuhpA showed significantly higher (p < 0.05) than fish infected with EIB202 at 24 h, 48 h, and 72 h after infection, and IFN-γ in spleen of fish infected with ΔuhpA showed significantly higher (p < 0.05) than fish infected with EIB202 at 12 h, 24 h and 72 h after infection. In summary, these results suggest that the uhpA gene deletion in E. piscicida affects Glu6P usage; most important, which could enhance the pathogenicity of E. piscicida in zebrafish, particularly increase the induction of the gene expression of IL-1β, TNF-α, IFN-γ and TGF-β in the spleens of zebrafish after infection.