Methionine Attenuates Lipopolysaccharide-Induced Inflammatory Responses via DNA Methylation in Macrophages
文献类型： 外文期刊
作者： Ji, Jian 1 ; Xu, Yibin 1 ; Zheng, Mingzhu 2 ; Luo, Chenglong 1 ; Lei, Huangtao 1 ; Qu, Hao 1 ; Shu, Dingming 1 ;
作者机构： 1.Guangdong Acad Agr Sci, State Key Lab Livestock & Poultry Breeding, Guangdong Key Lab Anim Breeding & Nutr, Inst Anim Sci, Guangzhou 510640, Guangdong, Peoples R China
2.NIAID, Mol & Cellular Immunoregulat Sect, Lab Immune Syst Biol, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA
期刊名称：ACS OMEGA （ 影响因子：3.512； 五年影响因子：3.613 ）
ISSN： 2470-1343
年卷期： 2019 年 4 卷 1 期
页码：
收录情况： SCI
摘要： Methionine (Met) is an essential and multifunctional nutrient in vertebrate diets. It is a precursor of S-adenosylmethionine (SAM), the methyl donor for DNA methylation, which has an important role in the inflammatory responses. However, whether Met exerts anti-inflammatory effects by altering DNA methylation in macrophages is unclear. In this study, Met was found to diminish the activation of the mitogen-activated protein kinase signaling pathway; decrease the production of tumor necrosis factor-a, interleukin-6, and interferon-beta; and enhance the levels of intracellular SAM after lipopolysaccharide (LPS) treatment in macrophages. Similarly, SAM inhibited the LPS-induced inflammatory response, consistent with the result of Met treatment. Met-treated macrophages displayed increased global DNA methylation. The DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine partially blocked the anti-inflammatory effects of Met in macrophages, suggesting a mechanism involving DNA methylation. Collectively, the results indicated that Met inhibits the LPS-induced inflammatory response by altering DNA methylation in RAW 264.7 macrophages. The findings provide new insights into the interplay between nutrition and immunology, and highlight the regulatory effects of amino acids on the host immune system.
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