研究报告

  • 柳燕贞,曾国驱.内分泌干扰素壬基酚对人THP-1巨噬细胞极化的影响[J].环境科学学报,2021,41(12):5229-5237

  • 内分泌干扰素壬基酚对人THP-1巨噬细胞极化的影响
  • The effects of 4-nonylphenol in THP-1 macrophage polarization
  • 基金项目:广东省重点领域研发计划项目(No.2020B202080005)
  • 作者
  • 单位
  • 柳燕贞
  • 1. 广东省科学院微生物研究所, 广东省微生物分析检测中心, 广州 510070;2. 华南应用微生物国家重点实验室, 广州 510070;3. 广东省菌种保藏与应用重点实验室, 广州 510070
  • 曾国驱
  • 1. 广东省科学院微生物研究所, 广东省微生物分析检测中心, 广州 510070;2. 华南应用微生物国家重点实验室, 广州 510070;3. 广东省菌种保藏与应用重点实验室, 广州 510070
  • 摘要:壬基酚(4-nonylphenol, NP)是一类典型的环境雌激素,能干扰机体正常免疫系统,对人类健康产生威胁.巨噬细胞是一类重要的免疫细胞,在调控组织稳态、炎症反应等方面发挥着重要作用,然而目前有关壬基酚对巨噬细胞极化和功能的影响尚不明确.本研究以人THP-1巨噬细胞为模型,采用不同浓度壬基酚(0、10、100 ng·mL-1)处理THP-1巨噬细胞,考察壬基酚对THP-1巨噬细胞增殖、迁移能力以及极化的影响.结果发现壬基酚处理对THP-1巨噬细胞的增殖无明显影响,但能增加THP-1巨噬细胞的迁移能力.壬基酚处理能显著促进M2型巨噬细胞标志物CD163和CD206的表达,上调细胞因子IL-10、Arg1、TGF-b的表达,下调细胞因子IL-12、iNOS的表达.Western Blot结果显示壬基酚处理能促进雌激素受体(Estrogen Receptor, ER)信号下游ERK1/2的磷酸化,ER拮抗剂ICI182780则能够逆转壬基酚对ERK1/2磷酸化的促进作用,并下调M2型巨噬细胞标志物CD163、CD206,以及细胞因子IL-10、TGF-b、Arg1的表达.以上研究表明,壬基酚通过激活雌激素受体信号促进人THP-1巨噬细胞向M2型极化,从而干扰机体免疫系统的功能.
  • Abstract:4-nonylphenol (NP) is an environmental estrogen, which interferes with the normal function of the immune system and poses a significant threat to human health. Macrophages are immune cells with important roles in regulating tissue homeostasis and inflammatory responses. However, the effect of nonylphenol on the macrophage polarization and function is still unclear. In this study, we investigated the effects of NP on THP-1 macrophage proliferation, migration and polarization. The results showed that treatment of NP significantly increased the migration of THP-1 macrophage, but has no effect on cell proliferation. Treatment of NP significantly increased the expression of M2-macrophage marker CD163 and CD206. Moreover, treatment of NP increased the expression of cytokines IL-10, Arg1 and TGF-b, but decreased the expression of cytokines IL-12 and iNOS. Western blot results showed that treatment of NP increased the phosphorylation level of ERK1/2. Furthermore, we found that treatment of ER inhibitor ICI182780 reversed NP-induced ERK1/2 phosphorylation, and decreased the expression of CD163, CD206, IF-10, TGF-b, and Arg1. Taken together, our results suggested that treatment of NP can induce M2-macrophage polarization via activation of ER signaling, thereby interfering with the normal function of the immune system.

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