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Metabolic-engineered probiotic- OMVs as nanovaccine mediating sequential immunomodulation for chronic bone infection immunotherapy

ABSTRACT: Lei et al. screen out Lactococcus lactis OMVs (Lac-OMVs) and develop metabolic-engineered NAD+-Lac-OMVs nanovaccine with potent tissue repair therapeutic effect. NAD+-Lac-OMVs sequentially activate dendritic cells by membrane component and reprogram inflammatory macrophages for anti-inflammation and bone repair by interior nicotinamide metabolites.

ORGANISM(S): Mus Musculus

SUBMITTER: Cao Yang

PROVIDER: PXD076052 | iProX | Mon Mar 23 00:00:00 GMT 2026

REPOSITORIES: iProX

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Metabolic-engineered probiotic-OMVs as nanovaccine mediating sequential immunomodulation for chronic bone infection immunotherapy

Project description:<p>Chronic, drug-resistant bone infection caused by methicillin-resistant Staphylococcus aureus (MRSA) features an immunosuppressive niche enabling persistent infection and impaired bone healing. Specific treatment requires initial antibacterial immune activation against infection, followed by reshaping an anti-inflammatory microenvironment for later bone repair. Here, we screen out Lactococcus lactis outer membrane vesicles (Lac-OMVs) with first-stage dendritic cells (DCs) activation and later-stage inflammatory macrophage repolarization potential. Mechanistically, enrichment of the nicotinamide metabolism pathway within Lac-OMVs is discovered, with nicotinamide adenine dinucleotide (NAD+) as a key anti-inflammatory mediator. NAD+-enriched Lac-OMVs (NAD+-Lac-OMVs) is thus metabolically engineered via targeted culture condition optimizing, exerting biphasic immunomodulatory effects: (i) Early-stage DCs activation establishes robust humoral immunity, protecting against primary and recurrent MRSA challenge (99.35 % and 98.07 % bacteria clearance each); (ii) Later-stage targeted NAD+ delivery reprograms inflammatory macrophages at defect site, resolving inflammation and establishing a pro-osteogenic microenvironment (~10 times higher bone-repair rate).</p>

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Project description:Nicotinamide adenine dinucleotide (NAD), a cofactor for hundreds of metabolic reactions in all cell types, plays an essential role in diverse cellular processes including metabolism, DNA repair, and aging. NAD metabolism is critical to maintain cellular homeostasis in response to environmental signals, however, how it is impacted by the environment remains unclear. Here, we report an unexpected trans-kingdom cooperation between bacteria and mammalian cells wherein bacteria contribute to host NAD biosynthesis. Bacteria confer mammalian cells with the resistance to inhibitors of NAMPT, the rate limiting enzyme in the main vertebrate NAD salvage pathway. Mechanistically, a microbial nicotinamidase (PncA) that converts nicotinamide to nicotinic acid, a key precursor in the alternative deamidated NAD salvage pathway, is necessary and sufficient for this protective effect. This bacteria-enabled bypass of the pharmacologically induced metabolic block in mammalian cells represents a novel paradigm in drug resistance. This host-microbe metabolic interaction also dramatically enhances the hepatic NAD-boosting efficiency of nicotinamide and nicotinamide riboside supplementation, demonstrating a crucial role of microbes, gut microbiota in particular, in systemic NAD metabolism.

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