Resolvin E1 regulates interleukin 23, interferon-γ and lipoxin A4 to promote the resolution of allergic airway inflammation
Resolvin E1 regulates interleukin 23, interferon-γ and lipoxin A4 to promote the resolution of allergic airway inflammation
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DOI：
10.1038/ni.1627
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发表时间：
2008-08-01
影响因子：
30.5
通讯作者：
Levy, Bruce D.
中科院分区：
文献类型：
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作者：
Haworth, Oliver;Cernadas, Manuela;Levy, Bruce D.
白细胞介素23（IL-23）是慢性炎症发病机制的组成部分。急性炎症的消退是由特定信号和介质如消退素E1（Resolvin E1，RvE 1）介导的主动过程。在这里，我们提供的证据表明，RvE 1，在纳克数量，促进炎症气道反应的解决，部分通过直接抑制IL-23和IL-6在肺中的生产。RvE 1治疗的促消退效应也与RvE 1治疗小鼠肺中较高浓度的干扰素-γ有关。我们的研究结果表明IL-23和IL-6在维持炎症中具有关键作用，它们促进产生IL-17的T辅助细胞的存活和分化，并确定了RvE 1启动的过敏性气道反应的解决方案。
Interleukin 23 (IL-23) is integral to the pathogenesis of chronic inflammation. The resolution of acute inflammation is an active process mediated by specific signals and mediators such as resolvin E1 (RvE1). Here we provide evidence that RvE1, in nanogram quantities, promoted the resolution of inflammatory airway responses in part by directly suppressing the production of IL-23 and IL-6 in the lung. Also contributing to the pro-resolution effects of RvE1 treatment were higher concentrations of interferon-gamma in the lungs of RvE1-treated mice. Our findings indicate a pivotal function for IL-23 and IL-6, which promote the survival and differentiation of IL-17-producing T helper cells, in maintaining inflammation and also identify an RvE1-initiated resolution program for allergic airway responses.