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首页> 外文期刊>Nature >Inflammatory memory sensitizes skin epithelial stem cells to tissue damage
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Inflammatory memory sensitizes skin epithelial stem cells to tissue damage

机译：炎症记忆使皮肤上皮干细胞对组织损伤敏感

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摘要

The skin barrier is the body's first line of defence against environmental assaults, and is maintained by epithelial stem cells (EpSCs). Despite the vulnerability of EpSCs to inflammatory pressures, neither the primary response to inflammation nor its enduring consequences are well understood. Here we report a prolonged memory to acute inflammation that enables mouse EpSCs to hasten barrier restoration after subsequent tissue damage. This functional adaptation does not require skin-resident macrophages or T cells. Instead, EpSCs maintain chromosomal accessibility at key stress response genes that are activated by the primary stimulus. Upon a secondary challenge, genes governed by these domains are transcribed rapidly. Fuelling this memory is Aim2, which encodes an activator of the inflammasome. The absence of AIM2 or its downstream effectors, caspase-1 and interleukin-1 beta, erases the ability of EpSCs to recollect inflammation. Although EpSCs benefit from inflammatory tuning by heightening their responsiveness to subsequent stressors, this enhanced sensitivity probably increases their susceptibility to autoimmune and hyperproliferative disorders, including cancer.
机译：皮肤屏障是人体抵抗环境侵害的第一道防线，由上皮干细胞（EpSC）维持。尽管EpSC易受炎症压力的影响，但人们对炎症的主要反应及其持久性后果均知之甚少。在这里，我们报告了对急性炎症的长时间记忆，使小鼠EpSC能够在随后的组织损伤后加快屏障恢复。这种功能适应性不需要皮肤驻留巨噬细胞或T细胞。相反，EpSC在主要刺激激活的关键应激反应基因上保持染色体可及性。在第二次攻击后，由这些结构域控制的基因会迅速转录。促进这种记忆的是Aim2，它编码炎性小体的激活剂。 AIM2或其下游效应子caspase-1和白介素1β的缺乏消除了EpSC收集炎症的能力。尽管EpSC通过增强其对后续应激源的反应性而从炎症调节中受益，但这种增强的敏感性可能会增加其对自身免疫和过度增殖性疾病（包括癌症）的敏感性。

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  • 来源
    《Nature》 |2017年第7677期|475-480|共6页
  • 作者

    Naik Shruti; Larsen Samantha B.; Gomez Nicholas C.; Alaverdyan Kirill; Sendoel Ataman; Yuan Shaopeng; Polak Lisa; Kulukian Anita; Chai Sophia; Fuchs Elaine;

  • 作者单位

    Rockefeller Univ, Howard Hughes Med Inst, Robin Chemers Neustein Lab Mammalian Cell Biol &, New York, NY 10065 USA;

    Rockefeller Univ, Howard Hughes Med Inst, Robin Chemers Neustein Lab Mammalian Cell Biol &, New York, NY 10065 USA;

    Rockefeller Univ, Howard Hughes Med Inst, Robin Chemers Neustein Lab Mammalian Cell Biol &, New York, NY 10065 USA;

    Rockefeller Univ, Howard Hughes Med Inst, Robin Chemers Neustein Lab Mammalian Cell Biol &, New York, NY 10065 USA;

    Rockefeller Univ, Howard Hughes Med Inst, Robin Chemers Neustein Lab Mammalian Cell Biol &, New York, NY 10065 USA;

    Rockefeller Univ, Howard Hughes Med Inst, Robin Chemers Neustein Lab Mammalian Cell Biol &, New York, NY 10065 USA;

    Rockefeller Univ, Howard Hughes Med Inst, Robin Chemers Neustein Lab Mammalian Cell Biol &, New York, NY 10065 USA;

    Rockefeller Univ, Howard Hughes Med Inst, Robin Chemers Neustein Lab Mammalian Cell Biol &, New York, NY 10065 USA;

    Rockefeller Univ, Howard Hughes Med Inst, Robin Chemers Neustein Lab Mammalian Cell Biol &, New York, NY 10065 USA;

    Rockefeller Univ, Howard Hughes Med Inst, Robin Chemers Neustein Lab Mammalian Cell Biol &, New York, NY 10065 USA;

  • 收录信息 美国《科学引文索引》(SCI);美国《工程索引》(EI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
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