Fig. 5: YfiD facilitates the pathogenicity of E. piscicida.

a YfiD inhibits the expression of proinflammatory genes during infection. Following DMSO and Olaparib pretreatment, J774A.1 cells were infected with E. piscicida WT or ΔyfiD, respectively. At 4 hpi, transcripts of IL-1α, IL-1β, and IL-6 were determined by RT-qPCR. b Statistical analysis of cell viability of J774A.1 cells infected with E. piscicida WT or ΔyfiD in the presence or absence of Olaparib at 6 hpi. c Intracellular survival of WT and ΔyfiD in J774A.1. Following the pretreatment of DMSO and Olaparib, J774A.1 cells were infected with WT and ΔyfiD at MOI 10. The number of intracellular bacteria was determined at 6 hpi. d Colonization of WT and ΔyfiD in turbots. The infection model was established by intraperitoneal injection of E. piscicida WT and ΔyfiD in turbots (10 per group) at a dose of 1×10⁶ CFUs/fish. At day 8 post-infection, CFUs from grinded livers, spleens, and kidneys were determined by plating on agar plates. e Percent survival of zebrafish (20 per group) was recorded for E. piscicida WT and ΔyfiD injection at a dose of 400 CFU/fish during a 7-day observation. All images shown are representative of three independent experiments (n = 3). ***, P < 0.001; **, P < 0.01; *, P < 0.05; ns, non-significance, P > 0.05 based on two-tailed Student’s t-test and Kaplan-Meier survival analysis with a log-rank test (Mantel-Cox).