Characterization of the molecular role that ST3GAL1 plays in porcine susceptibility to E. coli F18 infection.

Abstract

Escherichia coli F18 (E. coli F18) is the main cause of bacterial diarrhea in piglets. Previous transcriptome reported that ST3GAL1 was associated to E. coli F18 infection. However, its role in mediating the resistance to E. coli F18 remains elusive. Here, we revealed that the downregulation of ST3GAL1 expression contributed to the enhancement of E. coli F18 resistance in IPEC-J2 cells. Bisulfite sequencing identified 26 methylated CpG sites in the ST3GAL1 core promoter. Among these, the ST3GAL1 mRNA levels significantly correlated with methylation levels of the mC-8 site in the specificity protein 1 (SP1) transcription factor (P&#xa0;<&#xa0;0.01). Interestingly, ST3GAL1 expression may enhances the immune response by activating TLRs signaling, meanwhile decreases the production of the E. coli F18 receptor by inhibiting glycosphingolipid biosynthesis signaling, thereby leading to enhance the resistance to E. coli F18 infection. Besides, low ST3GAL1 expression may increase E. coli resistance by reducing sialylation. Together, these results support the status of ST3GAL1 as a viable target for efforts to modulate E. coli F18 susceptibility, offering a theoretical foundation for the use of this gene as a key biomarker for molecular breeding to improve porcine disease resistance.