Designed to remember

• 成果类型: Editorial Material
• 署名作者: Blot, Guillaume; Sapieha, Przemyslaw
• 署名单位: Universite de Montreal; Universite de Montreal
• 刊物名称: SCIENCE
• ISSN/ISSBN: 0036-8075; 1095-9203
• DOI: 10.1126/science.aeg3891
• 发表日期: 2026-03-26
• 页码: 1322-1323
• 关键词: INFLAMMATORY MEMORY

摘要

Inflammation is transient, but its consequences can be lifelong. Even brief episodes of inflammation can lead to long-lasting changes in chromatin that control gene expression. These changes can poise cells to respond differently to subsequent inflammation episodes. For example, an initial encounter with environmental stressors, such as bacteria, viruses, or Western diets, durably tunes innate immune responses to later (related or unrelated) challenges (1, 2). These mechanisms also exist in nonimmune cells, including the epidermal cells of human skin (3, 4). Why some inflammation-induced chromatin alterations are transient whereas others persist is unclear. On page 1347 of this issue, Cowley et al. (5) report that specific regions dense in cytosine and guanosine dinucleotides (CpG-rich) are epigenetically modified during inflammation to enable gene expression and that these changes persist during the animal's lifetime. The finding has implications for understanding how the genome determines the longevity of memory, which affects tissue fitness.