سامانه همایش های دانشگاه آزاد اسلامی واحد نجف آباد

صفحه اصلی / اولین همایش بین المللی تحول خدمات سلامت: تلفیق مراقبت، درمان، بازتوانی و امیدبخشی

The Amniotic Immune-Code: Deciphering How Human Amniotic Membrane-Derived Extracellular Vesicles Reprogram Macrophage Plasticity in Chronic Inflammation

نویسندگان :

Farshad Moharrami Kasmaie¹

1- دانشگاه علوم پزشکی اصفهان

کلمات کلیدی :

Amnion،Extracellular Vesicles،Macrophages،Inflammation،Wound Healing،Exosomes،Mesenchymal Stem Cells

چکیده :

Background: Macrophage plasticity governs the balance between chronic inflammation and tissue repair, and amniotic membrane-derived cells and their secretome have emerged as candidate modulators of this switch (1). The field lacks consensus on whether EV cargo or co-secreted soluble factors drive this reprogramming. Methods: This review synthesizes preclinical studies of human amnion epithelial cell (hAEC)-derived exosomes, amniotic conditioned medium, and amniotic membrane scaffolds on macrophage polarization markers, cytokine profiles, and tissue outcomes across pulmonary, renal, and cutaneous injury models. Findings: hAEC-derived exosomes shifted macrophages toward a CD206⁺ M2 phenotype while suppressing CD86⁺ M1 markers, increasing phagocytic activity and reducing neutrophil myeloperoxidase activity in bleomycin-induced lung fibrosis (2). Similar EV-mediated M2 polarization occurred in renal ischemia-reperfusion injury, with exosomal cargo enriched for extracellular matrix organization, growth factor signaling, and immunomodulatory proteins (3). This EV-dependence was not universal: conditioned medium from term-placenta amnion epithelial cells retained M2-polarising capacity after EV depletion, implicating soluble M-CSF rather than vesicular cargo, contrasting with prior work showing amnion-derived exosomes increasing CD206 expression (4). Human acellular amniotic membrane scaffolds loaded with exosomes suppressed wound inflammatory infiltrate and increased CD206⁺ macrophage recruitment in diabetic wounds (5). Conclusion: Amniotic membrane-derived EVs and secretome components consistently promote M2-like macrophage reprogramming, but the relative contribution of vesicular versus soluble mediators appears model- and preparation-dependent. Standardized fractionation protocols and cargo-level mechanistic studies are needed before clinical translation for chronic inflammatory disease.