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目的探讨IL-6协同M-CSF体外诱导CD14~+单核细胞向M2样巨噬细胞分化的作用机制,并检测诱导而来的M2样巨噬细胞的表型特点以及对肿瘤细胞的作用。方法体外构建IL-6诱导单核细胞分化模型,q RT-PCR检测M2表型分子(IL-10、TGF-β)在不同质量浓度IL-6刺激下的表达水平;Western blot检测STAT3信号通路的活化水平;采用细胞迁移、增殖实验验证IL-6诱导的M2样巨噬细胞对肿瘤细胞增殖、迁移的作用。结果在IL-6诱导分化的巨噬细胞中,IL-10、TGF-β表达增高呈IL-6剂量依赖性,且IL-6大量激活JAK/STAT3信号通路中的STAT3蛋白,使其磷酸化,si RNA沉默STAT3后,IL-10、TGF-β表达水平相应降低;此外,M2样巨噬细胞上清处理的实验组比对照组胃癌细胞增殖速度和迁移能力显著增强。结论 IL-6可以通过激活STAT3信号通路诱导单核细胞高表达IL-10、TGF-β,低表达IL-12的M2样巨噬细胞分化,并且M2样巨噬细胞可以促进肿瘤细胞的增殖和迁移。
Objective To investigate the mechanism of IL-6 and M-CSF inducing CD14 + monocytes to differentiate into M2-like macrophages in vitro and to detect the phenotypic characteristics of induced M2-like macrophages and their effect on tumor cells. Methods IL-6-induced monocyte differentiation model was established in vitro. The expression of M2 phenotype molecule (IL-10, TGF-β) under different concentrations of IL-6 was detected by q RT-PCR. Western blot was used to detect the expression of STAT3 signal pathway The activation and migration of M2-like macrophages induced by IL-6 were verified by cell migration and proliferation assays. Results In IL-6-induced macrophages, the expression of IL-10 and TGF-β increased in a dose-dependent manner and IL-6 significantly activated STAT3 in the JAK / STAT3 signaling pathway to phosphorylate , siRNA silence STAT3, IL-10, TGF-βexpression level correspondingly reduced; In addition, M2-like macrophage supernatant of the experimental group than the control group, the proliferation rate of gastric cancer cells and migration were significantly enhanced. Conclusion IL-6 can induce the differentiation of M2-like macrophages with high expression of IL-10, TGF-β, and low expression of IL-12 in monocytes by activating STAT3 signaling pathway. M2-like macrophages can promote tumor cell proliferation and migrate.