Bile acid- and taurocholate-mediated virulence in AHPND-causing Vibrio parahaemolyticus is independent of the LuxO-OpaR quorum sensing cascade

Acute hepatopancreatic necrosis disease (AHPND), a prevalent shrimp disease in Southeast Asia, is caused by a specific strain of Vibrio parahaemolyticus (VP) carrying a virulent pVA1 plasmid with PirAB^vp toxin genes. Several host and pathogenic factors affect AHPND pathogenesis. However, quorum sensing (QS), a cell density-based bacterial cell-to-cell communication that regulates virulence factors in Vibrios, mediated mechanisms of AHPND-causing VP are yet to be fully elucidated. Here, we used wild type V. parahaemolyticus, AHPND-causing strain 3HP, along with the 3HP LuxO and/or OpaR QS mutants (ΔopaRΔluxO, ΔopaR, ΔluxO, and luxO^D47E) to investigate the effects of bile acids and taurocholate, dietary supplements given to shrimp to improve growth, on the pathogenicity of AHPND-causing VP. Our results suggest that biofilm formation and PirAB^vp toxin release in AHPND-causing wild type and QS mutants VP strains were induced by bile acids and taurocholate. Furthermore, these dietary supplements affected genes related to flagellar apparatus (MotY, FlhB, FliK, flagellin), bacterial pilus (PilW), biofilm formation (VpsN), bile resistance (OmpT), quorum sensing (LuxR4425, LuxR2865, OpaR, LuxO) and PirAB^vp toxins (PirA, PirB). This suggests that bile acids or taurocholate may affect virulence mechanism of AHPND-causing VP in a LuxO-OpaR QS-independent manner. This study provided insights into host-pathogen interactions and molecular mechanisms of QS in biofilm formation and PirAB^vp toxin production in AHPND-causing VP.