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• BspE, a Brucella T4SS effector, promotes bacterial growth, survival in macrophages, and impacts inflammatory factor release. • It interacts with host PCBP1 in the nucleus, influencing P53 signaling, apoptosis inhibition, and Brucella replication. Brucella T4SS secretes numerous effector proteins to disrupt host immune responses and apoptosis, enabling long-term survival. One such effector protein is BspE, whose role remains largely unknown. In this study, we demonstrated that BspE promotes the growth of Brucella , enhances its survival in macrophages, and affects the release of macrophage inflammatory factors. Furthermore, BspE facilitates Brucella colonization and pathological damage in mice. Our findings reveal that BspE can be translated in the host cell nucleus, where it interacts with the host RNA-binding protein PCBP1 to promote Brucella replication in macrophages. Knockdown of PCBP1 affects BspE-mediated proliferation of Brucella in macrophages. Furthermore, the BspE-PCBP1 interaction hinders P53 signaling and inhibits macrophage apoptosis. Although this interaction affects inflammatory cytokines, it does not significantly involve the NF-κB pathway. These findings contribute to a better understanding of how the Brucella effector protein BspE regulates host immune responses and apoptosis to influence its own survival. [ABSTRACT FROM AUTHOR]