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首页> 外文期刊>Nature >Lipocalin 2 mediates an innate immune response to bacterial infection by sequestrating iron
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Lipocalin 2 mediates an innate immune response to bacterial infection by sequestrating iron

机译：脂蛋白2通过螯合铁介导对细菌感染的先天免疫应答

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Although iron is required to sustain life, its free concentration and metabolism have to be tightly regulated(1). This is achieved through a variety of iron-binding proteins including transferrin and ferritin(2). During infection, bacteria acquire much of their iron from the host by synthesizing siderophores that scavenge iron and transport it into the pathogen(3,4). We recently demonstrated that enterochelin, a bacterial catecholate siderophore, binds to the host protein lipocalin 2 (ref. 5). Here, we show that this event is pivotal in the innate immune response to bacterial infection. Upon encountering invading bacteria the Toll-like receptors on immune cells stimulate the transcription, translation and secretion of lipocalin 2; secreted lipocalin 2 then limits bacterial growth by sequestrating the iron-laden siderophore. Our finding represents a new component of the innate immune system and the acute phase response to infection.
机译：尽管铁是维持生命所必需的，但其自由浓度和新陈代谢必须受到严格的调节（1）。这是通过多种铁结合蛋白（包括转铁蛋白和铁蛋白）实现的（2）。在感染过程中，细菌通过合成铁离子清除铁并将其运输到病原体中，从而从宿主体内获取大量铁（3,4）。我们最近证明肠螯合素是一种细菌儿茶酚酸铁载体，与宿主蛋白lipocalin 2结合（参考文献5）。在这里，我们显示该事件在对细菌感染的固有免疫反应中至关重要。遇到入侵细菌时，免疫细胞上的Toll样受体刺激lipocalin 2的转录，翻译和分泌。分泌的lipocalin 2然后通过隔离铁载铁载体来限制细菌的生长。我们的发现代表了先天免疫系统的新组成部分以及对感染的急性期反应。

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