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Prolonged intracellular bacterial survival drives lipid metabolic remodeling in macrophages, leading to progressive accumulation of bis(monoacylglycero)phosphate (BMP), regulated by progranulin (PGRN). Mechanistically, PGRN maintains lysosomal homeostasis through direct interaction with BMP. PGRN deficiency disrupts lysosomal integrity, induces immunosuppressive polarization, and facilitates bacterial immune evasion. To address this, a dual\u2010targeting nanoparticle system (NPs@PGRN) targeting the \u201cPGRN\u2010BMP\u2010lysosome\u201d axis was developed. NPs@PGRN restores lysosomal bactericidal capacity via PGRN replenishment, significantly reduces bacterial burdens, and reprograms macrophage immunophenotypes toward antimicrobial competence. 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