Lipopolysaccharide Preconditioning Induces an Anti-inflammatory Phenotype in BV2 Microglia
Lipopolysaccharide Preconditioning Induces an Anti-inflammatory Phenotype in BV2 Microglia
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脂多糖预处理诱导 BV2 小胶质细胞抗炎表型
DOI：
10.1007/s10571-015-0324-1
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发表时间：
2016-11-01
影响因子：
4
通讯作者：
Cheng, Chun
中科院分区：
文献类型：
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作者：
Qin, Yongwei;Sun, Xiaolei;Cheng, Chun
越来越多的证据表明，内毒素耐受是对反复暴露于脂多糖(LPS)的一种基本的免疫稳态反应，它诱导巨噬细胞的反应性改变，导致促炎基因的表达受到抑制，介导炎症消退的因子表达增加。本研究采用实时定量聚合酶链式反应和免疫印迹技术检测BV2小胶质细胞M1和M2的表型变化。我们发现内毒素耐受时细胞因子和趋化因子的表达与M2极化时的细胞因子和趋化因子表达基本相似。免疫荧光双标记法进一步检测CD11b+BV2中M1和M2标志物的表达。内毒素耐受时M2标志物(CD206)表达增加，而M1(CD54)标志物表达降低。此外，不同转录因子的表达也不同，这些转录因子以调节促炎和抗炎反应而闻名。我们的数据表明，重复的内毒素治疗激活了一个分化程序，导致小胶质细胞向M2样表型极化。
Increasing evidence indicates that endotoxin tolerance is an essential immune-homeostatic response to repeated exposure to lipopolysaccharide (LPS) that induces a state of altered responsiveness in macrophage, resulting in repression of pro-inflammatory gene expression and increased expression of factors that mediate the resolution of inflammation. In this study, quantitative real-time polymerase chain reaction and Western blot for M1 and M2 markers were performed to characterize phenotypic changes of BV2 microglia. We found that the cytokine and chemokine expression during endotoxin tolerance were mostly similar to those found during M2 polarization. We further examined the expression of M1 and M2 markers in CD11b+BV2 by double immunofluorescent staining. The expression of M2 markers (CD206) increased, whereas the expression of M1 (CD54) markers reduced during endotoxin tolerance. Moreover, expression of different transcription factor, known for their function in the regulation of pro- and anti-inflammatory reaction, was also different. Our data demonstrate that repeat LPS treatment activates a differentiation program that leads to microglial polarization toward M2-like phenotype.