Faecalibacterium prausnitzii derived postbiotic attenuates PEDV-induced mitochondrial apoptosis through blocking viral entry.

Abstract

Porcine epidemic diarrhea virus (PEDV) damaged to the intestinal epithelial cells of suckling piglets, resulting in elevated mortality rates and substantial economic losses. This study aimed to evaluate the effect of F. prausnitzii on PEDV invasion and mitochondrial function in cells. Our study demonstrated that F. prausnitzii exhibited strongly adhesion to PEDV virions, thereby preventing their entry into cells and enhancing cell viability. Notably, F. prausnitzii inhibited PEDV-induced apoptosis in Vero-E6 cells, as indicated by decreased activation of PARP, caspase-3/9, and the Bax/Bcl-2 ratio, while preserving mitochondrial structure and membrane potential. Moreover, the adhesion-mediated inhibition of the PEDV-induced mitochondrial apoptotic pathway was correlated with reduced reactive oxygen species (ROS) production and cytochrome c translocation. These results suggested that F. prausnitzii as postbiotic may serve as a preventive measures against different subtype PEDV infection by targeting mitochondrial apoptotic pathways, and broadened the horizons for the antiviral effects of postbiotic.