• First identification of interaction between Brucella secretory protein VceA and host transcription factor FOXO1 via yeast two-hybrid and co-immunoprecipitation.
• VceA promotes FOXO1 nuclear translocation, shifting host macrophage metabolism toward glycolysis during Brucella abortus infection.
• Deletion of VceA (S2308-ΔVceA) reduces FOXO1 nuclear entry and glycolysis, confirming its critical role in metabolic reprogramming.
• Findings offer a novel rationale for metabolic therapeutic strategies against brucellosis and related intracellular infections.
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