Boros-Rausch Adam, Dorogin Anna, Nadeem Lubna, Shynlova Oksana, Lye Stephen James
Lunenfeld Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, ON M5G 1X5, Canada.
Department of Physiology, University of Toronto, Toronto, ON M5S 1A1, Canada.
Cells. 2025 Mar 30;14(7):514. doi: 10.3390/cells14070514.
The uterine smooth muscle (myometrium) is an immunomodulatory tissue capable of secreting multiple chemokines during pregnancy. We propose that before term labor, chemokines secreted as a result of mechanical stretch of the uterine walls by the growing fetus(es) induce infiltration of maternal monocytes into myometrium, drive their differentiation into macrophages, and induce pro-inflammatory (M1) polarization, leading to labor contractions. This study used high-throughput proteomic mass-spectrometry to investigate the underlying mechanisms and explored the therapeutic potential of a broad-spectrum chemokine inhibitor (BSCI, FX125L) in modulating these effects. Primary myocytes isolated from the myometrium of term pregnant women were subjected in vitro to static mechanical stretch. Proteomic analysis of stretched myocyte-conditioned media (CM) identified significant upregulation of chemokine-related pathways and ECM degradation proteins. CM induced in vitro differentiation of human monocytes to macrophages and polarization into an M1-like phenotype characterized by elevated ROS production. BSCI treatment altered the myocyte secretome, increasing tissue-remodeling and anti-inflammatory proteins, Annexin A1 and TGF-β. BSCI-treated myocyte secretions induced Annexin A1 expression in macrophages and enhanced their phagocytic activity. We conclude that factors secreted by mechanically stretched myocytes induce pro-inflammatory M1 macrophage polarization, while BSCI modulates myocyte secretome, which reprograms macrophages to a homeostatic M2-like phenotype, thus reducing inflammation. When treated with BSCI, M2-polarized macrophages reduced myocyte-driven collagen gel contraction, whereas M1 macrophages enhanced it. This study reveals novel insights into the myocyte-macrophage interaction and identifies BSCI as a promising drug to modulate myometrial activity. We suggest that uterine macrophages may represent a therapeutic target for preventing preterm labor in women.
子宫平滑肌(肌层)是一种免疫调节组织,在怀孕期间能够分泌多种趋化因子。我们提出,在足月分娩前,由于不断生长的胎儿对子宫壁的机械拉伸而分泌的趋化因子会诱导母体单核细胞浸润到肌层,促使它们分化为巨噬细胞,并诱导促炎(M1)极化,从而导致分娩宫缩。本研究使用高通量蛋白质组质谱法来研究其潜在机制,并探索一种广谱趋化因子抑制剂(BSCI,FX125L)在调节这些作用方面的治疗潜力。从足月孕妇的肌层分离出的原代肌细胞在体外进行静态机械拉伸。对拉伸后的肌细胞条件培养基(CM)进行蛋白质组分析,发现趋化因子相关途径和细胞外基质降解蛋白有显著上调。CM在体外诱导人单核细胞分化为巨噬细胞,并极化为以活性氧产生增加为特征的M1样表型。BSCI处理改变了肌细胞分泌组,增加了组织重塑和抗炎蛋白Annexin A1和转化生长因子-β。经BSCI处理的肌细胞分泌物诱导巨噬细胞中Annexin A1表达,并增强其吞噬活性。我们得出结论,机械拉伸的肌细胞分泌的因子诱导促炎M1巨噬细胞极化,而BSCI调节肌细胞分泌组,将巨噬细胞重新编程为稳态M2样表型,从而减轻炎症。用BSCI处理时,M2极化的巨噬细胞减少了肌细胞驱动的胶原凝胶收缩,而M1巨噬细胞则增强了这种收缩。本研究揭示了对肌细胞-巨噬细胞相互作用的新见解,并确定BSCI是一种有前景的调节子宫肌层活性的药物。我们认为子宫巨噬细胞可能是预防女性早产的治疗靶点。