Title : Edwardsiella piscicida induces largemouth bass PINK1/Parkin-mediated mitophagy for its survival and virulence
Abstract:
Edwardsiella piscicida (E. piscicida) is an intracellular pathogenic bacterium that widely infects aquatic animals, particularly fish, causing acute septicemia and local inflammation, ultimately leading to fish mortality. In recent years, mitophagy, an important mechanism for the clearance of damaged mitochondria within cells, has been demonstrated to play a key role in host cell immune responses. However, the interaction between E. piscicida and host mitophagy remains underexplored. This study reports for the first time that E. piscicida infection activates the PINK1/Parkin-mediated mitophagy pathway in the liver of Micropterus salmoides (largemouth bass). We explored the role of mitophagy in the host response to E. piscicida infection and its potential as a pathogenic immune evasion mechanism. The results showed that E. piscicida infection significantly upregulated the expression of mitophagy-related genes, including PINK1, Parkin, Beclin-1, LC3-II, and OPTN, which was confirmed both in vivo and in vitro. Transmission electron microscopy (TEM) revealed mitochondrial damage and the presence of autophagolysosomes. Additionally, PINK1 interference disrupted mitophagy, increased reactive oxygen species (ROS) levels, decreased bacterial load, and enhanced host survival, suggesting that E. piscicida may promote its survival by hijacking mitophagy. These findings indicate that the PINK1/Parkin-mediated mitophagy pathway is crucial for the immune evasion of E. piscicida and may serve as a novel therapeutic target for E. piscicida infections in fish.
