Exosomes derived from TGF-β1-modified mesenchymal stem cells protect septic mice by inducing macrophage M2 polarization

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Background Exosomes derived from mesenchymal stem cells (MSCs) have been reported to improve the prognosis in septic mice. Additionally, we have confirmed that TGF-β1 plays a critical role in MSC-mediated protection against sepsis. In this study, we aimed to investigate whether exosomes derived from TGF-β1-overexpressing MSCs (TGF-β1-Exo) offer protective effects in sepsis. Methods MSCs were collected from mouse MSCs stably transfected with TGF-β1 using a lentiviral vector. Exosomes were isolated and purified from MSCs (Exo), GFP-MSCs (GFP-Exo), and TGF-β1-MSCs (TGF-β1-Exo). A sepsis model was induced in mice via cecal ligation and perforation (CLP). After 6 h, exosomes from different sources were intravenously administered into septic mice. Mice were euthanised 24 h later, and histopathological changes were assessed using hematoxylin and eosin (H&E) staining. Inflammatory cytokine levels were measured using ELISA and RT-PCR. Flow cytometry was employed to evaluate macrophage phenotypes in lung tissues and in vitro macrophages. Additionally, we co-cultured fluorescently labeled exosomes with macrophages in vitro. Results TGF-β1-Exo significantly ameliorated histopathological damage and improved survival rates in septic mice. ELISA and RT-PCR analyses revealed that several pro-inflammatory cytokines were notably suppressed in the TGF-β1-Exo group. Furthermore, TGF-β1-Exo promote

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

Browse all related research

Filter the research library by this study's title keywords, author, or publication year.