Sodium taurocholate induces a colonization-adapted state in Vibrio parahaemolyticus by repressing acute virulence and promoting adhesion

Vibrio parahaemolyticus, a major seafood-borne pathogen, is exposed to bile salts such as sodium taurocholate (STC) during human infection. While bile salts are known to modulate virulence gene expression, their effects on biofilm formation and motility remain unclear. This study investigated the impact of subinhibitory STC (6.25 mM) on these phenotypes in V. parahaemolyticus RIMD2210633, testing the hypothesis that STC induces a colonization-adapted state, repressing acute virulence while promoting host-association traits. RNA sequencing revealed that STC altered the expression of 1176 genes (~ 24.3% of the genome). Our central finding is a coordinated transcriptional reprogramming characterized by the downregulation of key virulence determinants, including thermostable direct hemolysin (TDH) and multiple secretion systems (T3SS1, T3SS2 and T6SS1), alongside the upregulation of adhesion-related T6SS2 genes. Phenotypically, STC significantly suppressed cytotoxicity against HeLa cells but enhanced bacterial adhesion. While also affected motility and biofilm architecture—suppressing swimming motility, enhancing swarming, and reducing overall biofilm biomass despite upregulating some matrix genes—these phenotypes are interpreted as complementary adaptations supporting the overall colonization-adapted state. Collectively, these results indicate that sub-inhibitory STC reprograms V. parahaemolyticus physiology, repressing acute virulence mechanisms while promoting adhesion and surface adaptation through complex transcriptional and post-transcriptional mechanisms.