Burkholderia pseudomallei, the facultative intracellular pathogen that causes life-threatening melioidosis, delivers virulence effectors through secretion systems to subvert host-cell immunity, yet whether it deploys nuclear-targeted effectors to reprogram host immune responses remains unclear. Here, we identify BapC as a type III secretion system nucleomodulin that suppresses macrophage efferocytosis through epigenetic reprogramming. Mechanistically, BapC enters the host nucleus through an Asp95-dependent interaction with KPNB1. Nuclear BapC engages the Nucleosome Remodeling and Deacetylase (NuRD) complex to drive histone H3K18 deacetylation and repress efferocytosis-related genes. This epigenetic suppression impairs efferocytotic clearance of apoptotic cells by macrophages and promotes bacterial survival. Pharmacological inhibition of HDAC1/2, the deacetylase subunits of NuRD, restores efferocytosis and protects against lethal infection. Together, our study reveals how B. pseudomallei exploits a bacterial nucleomodulin to hijack a host chromatin corepressor complex and suppress innate immune clearance, suggesting HDAC inhibition as a potential host-directed therapeutic strategy for melioidosis.