H3K4me3
先天免疫系统
秀丽隐杆线虫
组蛋白
免疫
生物
组蛋白甲基化
甲基转移酶
获得性免疫系统
表观遗传学
组蛋白甲基转移酶
细胞生物学
甲基化
免疫学
DNA甲基化
遗传学
免疫系统
基因
发起人
基因表达
作者
Yi Xiao,Chao Han,Xiaocong Li,Xiao‐Feng Zhu,Sanhua Li,Nian Jiang,Changyan Yu,Yun Liu,Fang Liu
标识
DOI:10.1016/j.intimp.2024.111837
摘要
S-adenosylmethionine (SAM) was a methyl donor for modifying histones, which had crucial roles in lipid accumulation, tissue injury, and immune responses. SAM fluctuation might be linked to variations in histone methylation. However, the underlying molecular mechanisms of whether the SAM diet influenced the immune response via histone modification remained obscure. In this study, we utilized the Caenorhabditis elegans as a model to investigate the role of SAM diet in innate immunity. We found that 50 μM SAM increased resistance to Gram-negative pathogen Pseudomonas aeruginosa PA14 by reducing the bacterial burden in the intestine. Furthermore, through the genetic screening in C. elegans, we found that SAM functioned in germline to enhance innate immunity via an H3K4 methyltransferase complex to upregulate the immune response genes, including irg-1 and T24B8.5. Intriguingly, SAM also protected mice from P. aeruginosa PA14 infection by reducing the bacterial burden in lung. These findings provided insight into the mechanisms of molecular connections among SAM diet, histone modifications and innate immunity.
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