ArticleStem cells translational medicine2026
MSC-small extracellular vesicles alleviated Th2-airway inflammation by regulating the metabolism of DCs in mice.
Article in Stem cells translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundAllergic airway inflammation is one of the chronic inflammatory diseases and is generally dominated by T helper 2 cells (Th2). Dendritic cells (DCs) are essential to mounting the Th2-mediated airway inflammation by presenting inhaled antigens to prime CD4+ T cells. Small extracellular vesicles (sEV) derived from mesenchymal stem cells (MSCs) exhibited great interest in intractable diseases. However, the effects and mechanisms of MSC-sEV on DCs in airway inflammation is still unclear.
methodsWe isolated MSC-sEV using anion-exchange chromatography. Mouse bone marrow-derived DCs (BMDCs) and human monocyte-derived DCs (moDCs) were used to study the effects of MSC-sEV on dendritic cell surface molecules and their cytokine release. Mice were sensitized with house dust mites (HDM) to induce airway inflammation, and treated with MSC-sEV, the effects of sEV on murine DCs were identified. Extracellular flux analysis techniques were used to study the effects of MSC-sEV on the metabolic state of dendritic cells. RNA sequencing to study altered gene expression in BMDCs after MSC-sEV treatment.
resultsMSC-sEV mitigated the accumulation of Th2-associated cDC2s and moDCs in mouse lung in response to HDM. In vitro, MSC-sEV treatment significantly attenuated the activation of BMDCs. Furthermore, we identified that DCs were able to take MSC-sEV in vitro and in vivo. Mechanistically, MSC-sEV exerted regulatory effects on the metabolic pathways of murine DCs, specifically enhancing the reliance on oxidative phosphorylation of BMDCs. Importantly, MSC-sEV displayed similar effects on human moDCs.
conclusionsMSC-sEV are able to alter the metabolic state of DCs, favoring DCs to maintain OXPHOS (oxidative phosphorylation) rather than glycolysis, thereby reducing DCs-initiated inflammatory responses and attenuating Th2 lung inflammation, suggesting MSC-sEV can be a potential clinical therapy for airway inflammation.
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