Mechanism of exosomes from adipose-derived mesenchymal stem cells on sepsis-induced acute lung injury by promoting TGF-β secretion in macrophages.

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)

Objective Acute lung injury (ALI) caused by sepsis is a life-threatening condition characterized by uncontrollable lung inflammation. The current study sought to investigate the mechanism of adipose-derived mesenchymal stem cell-derived exosomes (ADMSC-Exos) in attenuating sepsis-induced ALI through TGF-β secretion in macrophages. Methods Adipose-derived mesenchymal stem cell-derived exosomes (ADMSC-Exos) were extracted from ADMSCs and identified. Septic ALI mouse models were established via cecal ligation and puncture (CLP), followed by administration of ADMSC-Exos or sh-TGF-β lentiviral vector. Mouse macrophages (cell line RAW 264.7) were treated with lipopolysaccharide (LPS), co-cultured with Exos and splenic T cells, and transfected with TGF-β siRNA. The lung injury of CLP mice was evaluated, and levels of inflammatory indicators and macrophage markers were measured. The localization of macrophage markers and TGF-β was determined, and the level of TGF-β in lung tissues was measured. The effect of TGF-β knockdown on sepsis-induced ALI in CLP mice was evaluated, and the percentages of CD4+CD25+Foxp3+ Tregs in mononuclear cells/macrophages and Foxp3 levels in lung tissues/co-cultured splenic T cells were examined. Results ADMSC-Exos were found to alleviate sepsis-induced ALI, inhibit inflammatory responses, and induce macrophages to secrete TGF-β in CLP mice. TGF-β silencing r

Evidence level

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

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