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Background <p>Human amniotic fluid stem cells (hAFSCs) secrete extracellular vesicles (EVs) that modulate fetal immunity. Because fetal and neonatal macrophages largely rely on innate responses, development of a targeted method to switch their inflammatory phenotype would fill a critical therapeutic gap in perinatal medicine. We therefore elucidated whether the hAFSC-EV surface marker CD44 functions as a “delivery code” for preferential uptake by inflammatory macrophages.</p> Methods and results <p>hAFSCs and hAFSC-EVs were isolated and characterized by performing flow cytometry, transmission electron microscopy, nanoparticle tracking analysis, and western blotting. The hAFSC-EVs were co-cultured with macrophages derived from the human monocytic leukemia cell line THP-1. The uptake of hAFSC-EVs was evaluated using fluorescence microscopy and flow cytometry. The effects of hAFSC-EVs on macrophages were analyzed by western blotting and real-time quantitative polymerase chain reaction. Our analyses revealed that inhibiting CD44 expression with a functional antibody blocked hAFSC-EV uptake by macrophages and led to changes in the cellular phenotype. Furthermore, inhibiting the uptake of CD44-positive hAFSC-EVs suppressed the expression of some pro-inflammatory cytokines. These findings suggest that CD44-positive hAFSC-EVs play a crucial role in the anti-inflammatory effects of hAFSCs.</p> Conclusions <p>Our study provides insights into the specific delivery of hAFSC-EVs into inflammatory macrophages and sheds light on the potential therapeutic applications of these EVs for regulating inflammatory macrophage phenotypes.</p>

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Extracellular vesicles released from human amniotic fluid stem cells modulate macrophages

  • 期刊论文

  • 发表日期：

    2025年9月18日

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  • Yushi Abe,
  • Daigo Ochiai,
  • Yosuke Matsumiya,
  • Seiji Kanzaki,
  • Mamoru Tanaka,
  • Manu Vatish

摘要

Background

Human amniotic fluid stem cells (hAFSCs) secrete extracellular vesicles (EVs) that modulate fetal immunity. Because fetal and neonatal macrophages largely rely on innate responses, development of a targeted method to switch their inflammatory phenotype would fill a critical therapeutic gap in perinatal medicine. We therefore elucidated whether the hAFSC-EV surface marker CD44 functions as a “delivery code” for preferential uptake by inflammatory macrophages.

Methods and results

hAFSCs and hAFSC-EVs were isolated and characterized by performing flow cytometry, transmission electron microscopy, nanoparticle tracking analysis, and western blotting. The hAFSC-EVs were co-cultured with macrophages derived from the human monocytic leukemia cell line THP-1. The uptake of hAFSC-EVs was evaluated using fluorescence microscopy and flow cytometry. The effects of hAFSC-EVs on macrophages were analyzed by western blotting and real-time quantitative polymerase chain reaction. Our analyses revealed that inhibiting CD44 expression with a functional antibody blocked hAFSC-EV uptake by macrophages and led to changes in the cellular phenotype. Furthermore, inhibiting the uptake of CD44-positive hAFSC-EVs suppressed the expression of some pro-inflammatory cytokines. These findings suggest that CD44-positive hAFSC-EVs play a crucial role in the anti-inflammatory effects of hAFSCs.

Conclusions

Our study provides insights into the specific delivery of hAFSC-EVs into inflammatory macrophages and sheds light on the potential therapeutic applications of these EVs for regulating inflammatory macrophage phenotypes.