<i>Edwardsiella piscicida</i> induces largemouth bass PINK1/Parkin-mediated mitophagy for its survival and virulence

PTEN-induced kinase 1 (PINK1)-mediated mitophagy, a classic mechanism underlying the elimination of damaged mitochondria, plays a crucial role in the immune evasion of bacteria. In the present study, we found that Edwardsiella piscicida, an intracellular pathogenic bacterium that infects fish, could induce PINK1-mediated mitophagy to enhance its survival and virulence in largemouth bass (Micropterus salmoides). E. piscicida infection damaged mitochondria in the liver or hepatocytes of largemouth bass and induced PINK1-mediated mitophagy, as confirmed by knockdown of PINK1, transmission electron microscopy, and qPCR analysis. Knockdown of PINK1 decreased the intracellular growth of E. piscicida and lowered the mortality rate of fish infected with E. piscicida. Additionally, qPCR revealed that knockdown of PINK1 increased the production of reactive oxygen species (ROS) and the expression levels of several immune-related genes, including piscidin-1, piscidin-3, TNF-α, TGF-β, and IL-10. Our results suggest that the PINK1-mediated pathway induced by E. piscicida may facilitate the survival of E. piscicida by inhibiting the production of ROS and regulating the expression of immune-related host genes. Our study provides new insights into the mechanism of immune escape of E. piscicida in largemouth bass.