Itaconate-based nanoparticles induce immunometabolic reprogramming in macrophages and alleviate diet-induced obesity

基于衣康酸的纳米颗粒可诱导巨噬细胞免疫代谢重编程,并缓解饮食诱导的肥胖。

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Abstract

Obesity is driven by chronic adipose tissue inflammation and macrophage dysfunction. Here, we report a cargo-free nanoparticle (NP) platform derived from itaconate-based polyesters (pITA-NPs) that reprograms macrophage immunometabolism and alleviates diet-induced obesity. pITA-NPs rapidly induce CD206 presentation through a translationally independent mechanism and drive a non-canonical M2-like transcriptional and metabolic state distinct from IL-4/STAT6 polarization, while restraining inflammatory activation and macrophage-adipocyte crosstalk to reduce lipid accumulation. Bioenergetic profiling revealed context-dependent metabolic tuning, with pITA-NPs promoting an M2-like metabolic transition in resting macrophages characterized by increased mitochondrial mass and oxidative phosphorylation, while inducing a metabolically restrained, quiescent-like state in M1-like macrophages. In obese mice, subcutaneous pITA-NP treatment suppresses weight gain, reduces adiposity, promotes adipose tissue beiging and brown fat activation, and mitigates systemic inflammatory responses. Together, these findings establish pITA-NPs as an effective immunometabolic nanotherapy that leverages materials-driven macrophage reprogramming and coordinates immune and metabolic regulation to treat obesity.

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