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血清素合成通过NAD+依赖蛋白质乙化维持巨细胞IL-1β的产生

Chuanlong Wang¹, Qingyi Chen¹, Siyuan Chen¹

¹State Key Laboratory of Swine and Poultry Breeding Industry, Guangdong Laboratory of Lingnan Modern Agriculture, College of Animal Science, South China Agricultural University, Guangzhou 510642, China.

|January 24, 2024

概括

由糖酸脱酶 (PHGDH) 调节的de novo血清合成,影响天生的免疫力. 在巨细胞中抑制PHGDH可降低IL-1β的产生和炎症反应,提供潜在的治疗点.

科学领域:

免疫代谢过程中的免疫代谢.
细胞的新陈代谢
具有天生的免疫力.

背景情况:

血清代谢影响免疫细胞功能,但其在新血清合成和先天免疫中的作用尚不清楚.
炎症性巨细胞表现出高糖酸脱酶 (PHGDH) 表达,这是de novo血清合成中的关键酶,由核因子 κB (NF-κB) 信号调节.

研究的目的:

研究新型血清蛋白合成在先天性免疫细胞功能中的作用,特别关注巨细胞介质蛋白 (IL) - 1β的产生.
阐明PHGDH调节IL-1β产生和炎症反应的分子机制.

主要方法:

在巨细胞中抑制PHGDH的药理学抑制和基因调节.
评估IL-1β的产生,NAD+水平和SIRT1/SIRT3活动.
对表观遗传修饰 (H3K9/27乙化) 和炎症酶激活 (NLRP3) 的分析.
在体内研究中,在脂多糖引起的炎症期间,小鼠患有骨髓细胞特异性Phgdh缺乏症.

主要成果:

抑制或消耗PHGDH可降低巨细胞中的IL-1β产生.
PHGDH调节导致NAD+积累,增强NAD+依赖的SIRT1和SIRT3活动.
通过对Toll类受体4 (TLR4) 的表观遗传调节,PHGDH维持了IL-1β的表达,并通过NLRP3炎症酶激活促进了IL-1β的成熟.
骨髓特异性Phgdh缺乏的小鼠在体内表现出减弱的炎症反应.

结论:

由PHGDH介导的De novo血清合成在调节先天免疫细胞中的IL-1β产生方面发挥着关键作用.
通过表观遗传修饰和炎症酶激活,PHGDH会影响IL-1β的产生.
向PHGDH代表了对炎症性疾病的潜在治疗策略.

关键词:

这是NAD (((+)在NLRP3中,NLRP3是NLRP3中的一个.PHGDH PHGDH 的时间一个SIRT1系统.在SIRT3中,SIRT3是最重要的.在 TLR4 中,通过乙化处理.巨细胞是一个巨细胞.血清蛋白质是什么血清蛋白质

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