Institute of Molecular and Cell Biology (IMCB), Agency for Science, Technology and Research (A*STAR), 61 Biopolis Drive, Proteos, Singapore 138673, Singapore.
Paracrine Therapeutics Pte. Ltd., 10 Choa Chu Kang Grove #13-22 Sol Acres, Singapore 688207, Singapore.
Biomolecules. 2023 Oct 10;13(10):1501. doi: 10.3390/biom13101501.
Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by joint inflammation and damage, often associated with an imbalance in M1/M2 macrophages. Elevated levels of anti-inflammatory M2 macrophages have been linked to a therapeutic response in RA. We have previously demonstrated that mesenchymal stem/stromal cell small extracellular vesicles (MSC-sEVs) promote M2 polarization and hypothesized that MSC-sEVs could alleviate RA severity with a concomitant increase in M2 polarization. Here, we treated a mouse model of collagen-induced arthritis (CIA) with MSC-sEVs. Relative to vehicle-treated CIA mice, both low (1 μg) and high (10 μg) doses of MSC-sEVs were similarly efficacious but not as efficacious as Prednisolone, the positive control. MSC-sEV treatment resulted in statistically significant reductions in disease progression rate and disease severity as measured by arthritic index (AI), anti-CII antibodies, IL-6, and C5b-9 plasma levels. There were no statistically significant differences in the treatment outcome between low (1 μg) and high (10 μg) doses of MSC-sEVs. Furthermore, immunohistochemical analysis revealed that concomitant with the therapeutic efficacy, MSC-sEV treatment increased anti-inflammatory M2 macrophages and decreased pro-inflammatory M1 macrophages in the synovium. Consistent with increased M2 macrophages, histopathological examination also revealed reduced inflammation, pannus formation, cartilage damage, bone resorption, and periosteal new bone formation in the MSC-sEV-treated group compared to the vehicle group. These findings suggest that MSC-sEVs are potential biologic disease-modifying antirheumatic drugs (DMARDs) that can help slow or halt RA joint damage and preserve joint function.
类风湿关节炎(RA)是一种慢性自身免疫性疾病,其特征为关节炎症和损伤,通常与 M1/M2 巨噬细胞失衡有关。抗炎性 M2 巨噬细胞水平升高与 RA 的治疗反应有关。我们之前已经证明,间充质干细胞/基质细胞小细胞外囊泡(MSC-sEVs)促进 M2 极化,并假设 MSC-sEVs 可以通过增加 M2 极化来减轻 RA 的严重程度。在这里,我们用 MSC-sEVs 治疗胶原诱导性关节炎(CIA)的小鼠模型。与 vehicle 处理的 CIA 小鼠相比,低(1μg)和高(10μg)剂量的 MSC-sEVs 同样有效,但不如阳性对照Prednisolone 有效。MSC-sEV 治疗可使疾病进展率和疾病严重程度(通过关节炎指数(AI)、抗 CII 抗体、IL-6 和 C5b-9 血浆水平测量)显著降低。低(1μg)和高(10μg)剂量的 MSC-sEVs 之间的治疗效果没有统计学上的显著差异。此外,免疫组织化学分析显示,与治疗效果一致,MSC-sEV 治疗增加了滑膜中的抗炎性 M2 巨噬细胞,减少了促炎性 M1 巨噬细胞。与 M2 巨噬细胞增加一致,组织病理学检查还显示 MSC-sEV 治疗组与 vehicle 组相比,炎症、血管翳形成、软骨损伤、骨吸收和骨膜新骨形成减少。这些发现表明,MSC-sEVs 是潜在的生物性疾病修饰抗风湿药物(DMARDs),可以帮助减缓或阻止 RA 关节损伤并保持关节功能。