Bacteriophages as viral predators can restrict host strains and shape the bacterial community. Conversely, bacteria also adopt diverse strategies for phage defense. Pseudomonas syringae pv. actinidiae (Psa) is the causal agent of bacterial canker on kiwifruit. Though Psa lacks quorum sensing signaling molecule synthase LuxI, two (PsaR1 and PsaR3) of three LuxR homologous were confirmed to bind with exogenous N-acyl homoserine lactone (AHL), OXO-C8-HSL. The adsorption and infection efficiency of phage KBC54 to Psa significantly reduced by adding OXO-C8-HSL or heterologous expression of traI of Agrobacterium tumefaciens in Psa. By generating PsaR1 and PsaR3 mutants, as well as PsaR-AHL MST assays, we specified that the two PsaRs can recruit AHL to enhance bacterial resistance against phage. Absence of PsaR1 and PsaR3 resulted in up-regulation of the outer membrane protein OmpV, and knockout of ompV led to impaired phage adsorption efficiency. Given that OmpV specifically interacted with the phage tail fiber protein Tp3 in pull-down assay, we deduced that OmpV serves as a cell surface receptor recognized by phage. This study highlights the remarkable ability of Psa recruiting QS signals to inhibit phage infection. This may be a common strategy for non-AHL producing bacteria that evolved to take control of phage infection and promote host fitness by orchestrating QS signals in living niches.