The hallmarks of allergic airway disease (AAD) include infiltration of inflammatory cells into the bronchoalveolar space. Bone marrow derived mesenchymal stem cells (BMSCs) show anti-inflammatory properties in AAD. In addition, galectin-1 (Gal-1) is a lectin significantly upregulated upon inflammation and is also known to mediate potential anti-inflammatory responses. We hypothesized that BMSCs regulated inflammatory responses by secretion of Gal-1 during AAD pathogenesis. BMSCs were isolated from murine femurs and tibiae and adoptively transferred into an ovalbumin-induced AAD mouse model. Knockdown of Gal-1 in BMSCs was performed using shRNA. Flow cytometry, ELISAs, and immunohistology were performed to analyze inflammatory responses in mice, and a Transwell system was used to establish an in vitro co-culture system of lung epithelial cells (MLE-12) and BMSCs. Administration of BMSCs significantly upregulated Gal-1 expression upon inflammation and decreased infiltration of inflammatory cells and secretion of proinflammatory cytokines in vivo. In addition, we showed that this function was mediated by reduced activation of the MAPK p38 signaling pathway. Similar observations were found using an in vitro lipopolysaccharide-induced model when MLE-12 cells were co-cultured with BMSCs. Gal-1 secretion by BMSCs alleviated inflammatory responses observed in AAD and hence provides a promising therapeutic alternative to AAD patients insensitive to conventional drug treatments.

过敏性气道疾病（AAD）的特征包括炎症细胞浸润到支气管肺泡腔。骨髓间充质干细胞 (BMSC) 在 AAD 中表现出抗炎特性。此外，半乳糖凝集素-1 (Gal-1) 是一种在炎症时显着上调的凝集素，并且还已知可介导潜在的抗炎反应。我们假设 BMSC 在 AAD 发病过程中通过分泌 Gal-1 来调节炎症反应。从小鼠股骨和胫骨中分离出 BMSC，并过继转移至卵清蛋白诱导的 AAD 小鼠模型中。使用 shRNA 敲低 BMSC 中的 Gal-1。采用流式细胞术、ELISA和免疫组织学分析小鼠炎症反应，并利用Transwell系统建立肺上皮细胞（MLE-12）和BMSCs的体外共培养体系。 BMSCs 的施用显着上调炎症时 Gal-1 的表达，并减少体内炎症细胞的浸润和促炎细胞因子的分泌。此外，我们发现该功能是通过减少 MAPK p38 信号通路的激活来介导的。当 MLE-12 细胞与 BMSC 共培养时，使用体外脂多糖诱导模型发现了类似的观察结果。 BMSC 分泌的 Gal-1 减轻了 AAD 中观察到的炎症反应，因此为对常规药物治疗不敏感的 AAD 患者提供了一种有前途的治疗替代方案。