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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >The Nalp3 Inflammasorne Is Essential For The Development Of Silicosis
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The Nalp3 Inflammasorne Is Essential For The Development Of Silicosis

机译：Nalp3 Inflammasorne对矽肺病的发展至关重要

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Inhalation of crystalline silica and asbestos is known to cause the progressive pulmonary fibrotic disorders silicosis and asbestosis, respectively. Although alveolar macrophages are believed to initiate these inflammatory responses, the mechanism by which this occurs has been unclear. Here we show that the inflammatory response and subsequent development of pulmonary f ibrosis after inhalation of silica is dependent on the Nalp3 inflammasome. Stimulation of macrophages with silica results in the activation of caspase-1 in a Nalp3-dependent manner. Macrophages deficient in components of the Nalp3 inflammasome were incapable of secreting the proinflammatory cytokines interleukin (IL)-1β and IL-18 in response to silica. Similarly, asbestos was capable of activating caspase-1 in a Nalp3-dependent manner. Activation of the Nalp3 inflammasome by silica required both an efflux of intracellular potassium and the generation of reactive oxygen species. This study demonstrates a key role for the Nalp3 inflammasome in the pathogenesis of pneumoconiosis.
机译：吸入结晶二氧化硅和石棉已知分别引起进行性肺纤维化疾病矽肺和石棉沉着。尽管认为肺泡巨噬细胞会引发这些炎症反应，但尚不清楚其发生的机制。在这里，我们显示了吸入二氧化硅后的炎症反应和随后肺纤维化的发展取决于Nalp3炎症小体。用二氧化硅刺激巨噬细胞导致caspase-1以Nalp3依赖性方式活化。缺乏Nalp3炎性小体成分的巨噬细胞不能响应二氧化硅而分泌促炎细胞因子白介素（IL）-1β和IL-18。同样，石棉能够以依赖Nalp3的方式激活caspase-1。二氧化硅激活Nalp3炎性小体既需要胞内钾的流出，又需要产生活性氧。这项研究表明，Nalp3炎性小体在尘肺病的发病机理中具有关键作用。

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