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Plos Pathog:酰基羧酸水解酶促进脂多糖诱导的急性肺损伤的消退

2017-06-20 MedSci MedSci原创

我们报告了AOAH以前不了解的促进LPS或革兰氏阴性细菌诱导的肺损伤的消退的作用。除了许多其他预分解机制,我们的研究表明,灭活MAMP分子对于从MAMP诱导的肺损伤中恢复是至关重要的。促进组织中LPS和其他MAMP分子降解的干预可促进炎症的消除。

肺部感染是急性肺损伤(ALI)的最常见的危险因素。由微生物相关分子模式(MAMP)分子诱导的先天免疫应答对于肺部防御是必不可少的,但可导致组织损伤。我们对关于MAMP分子如何在肺中降解或MAMP降解/失活如何有助于预防或改善产生ALI的有害炎症等知之甚少。酰基羧酸水解酶(AOAH)是使革兰氏阴性细菌内毒素(脂多糖或LPS)失活的宿主脂肪酶。我们在这里报道,肺泡巨噬细胞暴露于LPS后增加AOAH表达,并且由鼻内滴注的LPS或肺炎克雷伯氏杆菌诱导的ALI的Aoah + / +小鼠比Aoah - / - 小鼠恢复更快。Aoah - / - 小鼠肺具有更持续的白细胞浸润,更多的促炎细胞因子表达和持久的肺泡屏障损伤。我们还报导了Aoah - / - 肺泡中持续生物活性的LPS可以直接刺激肺泡巨噬细胞和间接刺激细胞上皮细胞,并导致产生将嗜中性粒细胞募集到肺部并可能阻止其清除的化学引诱物的证据。与LPS暴露的Aoah - / - 腹膜巨噬细胞中观察到的长期耐受性不同,缺乏AOAH的肺泡巨噬细胞维持或增加其对生物活性LPS的反应并持续发炎。AOAH导致的LPS的失活是可以使由革兰阴性细菌感染引起的肺部炎症/损伤消退的以前未被认可的机制。

结论:我们报告了AOAH以前不了解的促进LPS或革兰氏阴性细菌诱导的肺损伤的消退的作用。除了许多其他预分解机制,我们的研究表明,灭活MAMP分子对于从MAMP诱导的肺损伤中恢复是至关重要的。促进组织中LPS和其他MAMP分子降解的干预可促进炎症的消除。

原文出处:

Benkun Zou,Wei Jiang,Han Han,et al.Acyloxyacyl hydrolase promotes the resolution of lipopolysaccharide-induced acute lung injury.[J]Published: June 16, 2017,https://doi.org/10.1371/journal.ppat.1006436

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    2017-06-22 tastas

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