Engineered macrophage membrane-coated dihydroartemisinin nanoparticles with enhanced CCR2 expression improved symptoms in MRL/LPR mice by metabolic reprogramming of proinflammatory macrophages

通过增强CCR2表达,工程化巨噬细胞膜包覆的二氢青蒿素纳米颗粒通过促炎巨噬细胞的代谢重编程改善了MRL/LPR小鼠的症状。

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Abstract

BACKGROUND: Systemic lupus erythematosus (SLE) is a debilitating autoimmune condition characterized by limited therapeutic options. Dihydroartemisinin (DHA), an antimalarial compound, exhibits promising immunomodulatory effects against SLE; however, its clinical application is limited by poor bioavailability. METHODS: This study presented an innovative DHA delivery system based on macrophage membrane-coated nanoparticles (CCR2-MM@PEG-PCL/DHA), engineered to target SLE and its severe renal manifestation, lupus nephritis (LN). CCL2, a central mediator of leukocyte chemotaxis, contributes significantly to SLE pathogenesis. The targeting ability of nanoparticles to inflammatory sites is enhanced by genetically modifying the membrane of macrophages to over-express CCR2, and the nanoparticles can act as "nanobait" to capture CCL2 in the inflammatory microenvironment, thereby inhibiting macrophage-mediated inflammation. Efficacy was evaluated in vitro and in vivo using the MRL/lpr murine model. RESULTS: The findings showed that this nanosystem effectively alleviated symptoms in the MRL/lpr mouse model of SLE. Furthermore, CCR2-MM@PEG-PCL/DHA modulated the renal immune microenvironment by reducing monocyte/macrophage infiltration and reprogramming the M1/M2 macrophage balance, thus mitigating kidney damage in SLE mice. CONCLUSIONS: The study establishes a mechanistically informed strategy for SLE intervention, substantiated by robust in vitro and in vivo data. These findings lay the foundation for translational research and potential clinical advancement in SLE therapy.

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