酸作为一种依赖于食状态的调节代谢物,以对抗与营养负载和肥胖相关的促炎信号
Kim Han1, Allison M Meadows1,2, Matthew J Rodman1
1Laboratory of Mitochondrial Biology and Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Room 5-3342, Bld 10-CRC, 10 Center Drive, Bethesda, MD 20817, United States.
Journal of leukocyte biology
|January 11, 2024
概括
禁食和再食通过像酸这样的代谢物调节免疫反应. 这种短链脂肪酸 (SCFA) 和它的受体 (ffar2) 抑制CD4+T细胞炎症,为免疫调节提供了洞察力.
科学领域:
- 免疫学 免疫学 免疫学
- 代谢学 代谢学 代谢学
- 生物信息学是一种生物信息学.
背景情况:
- 禁食和再食调节人类的免疫反应,特别是CD4+ T细胞.
- 关联营养摄入与免疫细胞调节的确切机制尚未完全理解.
研究的目的:
- 为了确定受营养负载影响的代谢物驱动的免疫调节途径.
- 研究短链脂肪酸 (SCFA) 在禁食和再养期间调节CD4+T细胞反应中的作用.
主要方法:
- 综合生物信息学分析RNA测序和质谱数据.
- 测量血清代谢物和外围血液单核细胞基因表达在人类志愿者进行禁食和再养.
- 在体外实验中使用CD4+T细胞,酸和G蛋白结合受体43 (ffar2) 激动剂/对抗剂.
主要成果:
- 酸,SCFA和ffar2被禁食和重新养反向调节.
- propionate 和 ffar2 激动剂降低了 CD4+ T 细胞中的促炎性细胞因子 (干扰素-γ,介质素-17),基因素脱乙酶活性,核因子 κB 活性和介质素-6 释放.
- 酸抑制了STAT1和STAT3酸化和CD4+T细胞激活,包括来自肥胖个体的细胞.
结论:
- 一个涉及SCFA,特别是酸和ffar2等G蛋白结合受体的营养负载响应途径,调节CD4+T细胞免疫反应.
- 这种途径在缓解炎症方面发挥着作用,在诸如肥胖等与轻度炎症相关的疾病中可能是相关的.
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