Bile acid- and taurocholate-mediated virulence in AHPND-causing Vibrio parahaemolyticus is independent of the LuxO-OpaR quorum sensing cascade
Journal
Aquaculture
Journal Volume
606
Start Page
742604
ISSN
0044-8486
Date Issued
2025-08-15
Author(s)
Kumar, Ramya
Lin, Shin-Jen
Wang, Hao-Ching
Fagutao, Fernand F.
Wang, Han-Ching
Abstract
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 PirABvp 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 luxOD47E) 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 PirABvp 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 PirABvp 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 PirABvp toxin production in AHPND-causing VP.
Subjects
AHPND
Bile acids
Quorum sensing
Taurocholate
V. parahaemolyticus
SDGs
Publisher
Elsevier BV
Type
journal article