Quorum Sensing Positively Regulates CPS-dependentAutographiviridaePhages Infection inVibrio alginolyticus

Abstract

ABSTRACTQuorum sensing (QS) orchestrates many bacterial behaviors, such as virulence and biofilm formation, across bacterial populations. Nevertheless, the underlying mechanism of QS regulating CPS-dependent phage-bacterium interactions remains unclear. In the present study, we report that QS upregulated the expression of CPS-dependent phage receptors, thus increasing phage adsorption and infection rates inV. alginolyticus. We found that QS upregulated the expression of theugdgene, leading to increased synthesis ofAutographiviridaephage receptor capsular polysaccharide (CPS) synthesis inV. alginolyticus. The signal molecule autoinducer-2 (AI-2) released byV. alginolyticusfrom different sources can potentially enhance CPS-dependent phage infection. Therefore, our data suggest that inhibiting quorum sensing may reduce rather than improve the therapeutic efficacy of CPS-specific phages.IMPORTANCEPhage resistance is a direct threat to phage therapy, and understanding phage-host interactions, especially bacteria block phage infection, is essential for developing successful phage therapy. In the present study, we demonstrate for the first time thatV. alginolyticususes QS to promote CPS-specific phage infection by upregulating the expression ofugd, which is necessary for the synthesis ofAutographiviridaephage receptor capsular polysaccharide (CPS). Although increased CPS-specific phage susceptibility is a novel trade-off mediated by QS, it results in the upregulation of virulence factors, promoting biofilm development and enhanced capsular polysaccharide production inV. alginolyticus. This suggests that inhibiting QS may improve the effectiveness of antibiotic treatment, but it may also reduce the efficacy of phage therapy.