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Histone hyperacetylation mediates enhanced IL-1β production in LPS/IFN-γ-stimulated macrophages.
Immunology ( IF 6.4 ) Pub Date : 2020-04-07 , DOI: 10.1111/imm.13183 Zhen Dong 1 , Ruoshui Li 2 , Lei Xu 1 , Kaiyue Xin 1 , Yamei Xu 1 , Haiming Shi 2 , Aijun Sun 1, 3 , Junbo Ge 1, 3
Immunology ( IF 6.4 ) Pub Date : 2020-04-07 , DOI: 10.1111/imm.13183 Zhen Dong 1 , Ruoshui Li 2 , Lei Xu 1 , Kaiyue Xin 1 , Yamei Xu 1 , Haiming Shi 2 , Aijun Sun 1, 3 , Junbo Ge 1, 3
Affiliation
Under the condition of lipopolysaccharide (LPS)/interferon (IFN)-γ activation, macrophage metabolism is converted from oxidative phosphorylation to glycolysis. In the present work, we analysed whether glycolysis could affect interleukin (IL)-1β expression through altering histone acetylation levels in mouse bone marrow-derived macrophages. Immunocytochemistry and Western blot analysis are used to characterize histone acetylation in macrophages stimulated by LPS/IFN-γ. Real-time polymerase chain reaction and enzyme-linked immunosorbent assay were used to determine IL-1β production. The metabolism of macrophages was monitored in real-time by the Seahorse test. Our results showed that glycolytic metabolism could enhance histone acetylation and promote IL-1β production in LPS/IFN-γ-activated macrophages. Moreover, increased production of IL-1β by glycolysis was mediated through enhanced H3K9 acetylation. Importantly, it was found that a high dose of histone deacetylase inhibitor could also significantly increase the expression of IL-1β in the absence of glycolytic metabolism. In conclusion, this study demonstrates that glycolytic metabolism could regulate IL-1β expression by increasing histone acetylation levels in LPS/IFN-γ-stimulated macrophages.
中文翻译:
组蛋白超乙酰化介导了LPS /IFN-γ刺激的巨噬细胞中IL-1β产生的增强。
在脂多糖(LPS)/干扰素(IFN)-γ活化的条件下,巨噬细胞代谢从氧化磷酸化转化为糖酵解。在当前的工作中,我们分析了糖酵解是否可以通过改变小鼠骨髓来源的巨噬细胞中的组蛋白乙酰化水平来影响白介素(IL)-1β表达。免疫细胞化学和蛋白质印迹分析被用来表征LPS /IFN-γ刺激的巨噬细胞中的组蛋白乙酰化。实时聚合酶链反应和酶联免疫吸附试验用于确定IL-1β的产生。通过海马测试实时监测巨噬细胞的代谢。我们的结果表明,糖酵解代谢可以增强组蛋白乙酰化并促进LPS /IFN-γ活化的巨噬细胞中IL-1β的产生。此外,通过增强的H3K9乙酰化介导糖酵解增加IL-1β的产生。重要的是,发现在不存在糖酵解代谢的情况下,高剂量的组蛋白脱乙酰基酶抑制剂也可以显着增加IL-1β的表达。总之,这项研究表明糖酵解代谢可以通过增加LPS /IFN-γ刺激的巨噬细胞中的组蛋白乙酰化水平来调节IL-1β的表达。
更新日期:2020-04-07
中文翻译:
组蛋白超乙酰化介导了LPS /IFN-γ刺激的巨噬细胞中IL-1β产生的增强。
在脂多糖(LPS)/干扰素(IFN)-γ活化的条件下,巨噬细胞代谢从氧化磷酸化转化为糖酵解。在当前的工作中,我们分析了糖酵解是否可以通过改变小鼠骨髓来源的巨噬细胞中的组蛋白乙酰化水平来影响白介素(IL)-1β表达。免疫细胞化学和蛋白质印迹分析被用来表征LPS /IFN-γ刺激的巨噬细胞中的组蛋白乙酰化。实时聚合酶链反应和酶联免疫吸附试验用于确定IL-1β的产生。通过海马测试实时监测巨噬细胞的代谢。我们的结果表明,糖酵解代谢可以增强组蛋白乙酰化并促进LPS /IFN-γ活化的巨噬细胞中IL-1β的产生。此外,通过增强的H3K9乙酰化介导糖酵解增加IL-1β的产生。重要的是,发现在不存在糖酵解代谢的情况下,高剂量的组蛋白脱乙酰基酶抑制剂也可以显着增加IL-1β的表达。总之,这项研究表明糖酵解代谢可以通过增加LPS /IFN-γ刺激的巨噬细胞中的组蛋白乙酰化水平来调节IL-1β的表达。