Contribution of NOD2 to lung inflammation during Staphylococcus aureus-induced pneumonia
Contribution of NOD2 to lung inflammation during Staphylococcus aureus-induced pneumonia
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DOI：
10.1016/j.micinf.2010.05.003
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发表时间：
2010-09-01
影响因子：
5.8
通讯作者：
Adib-Conquy, Minou
中科院分区：
文献类型：
--
作者：
Kapetanovic, Ronan;Jouvion, Gregory;Adib-Conquy, Minou
金黄色葡萄球菌是重症监护病房患者中最常见的革兰氏阳性细菌，可引起败血症或肺炎。在这项工作中，我们研究了NOD 2在S.金黄色葡萄球菌引起的肺炎我们发现NOD 2的缺乏影响了体重减轻和恢复速度。与野生型动物相比，Nod 2-/-小鼠表现出减少的肺部炎症，支气管肺泡灌洗液中细胞因子的存在较低，中性粒细胞的募集减少。此外，肺部的组织学分析显示，在感染后第2天和第7天，Nod 2-/-小鼠的病变不太严重。总之，我们证明了NOD 2不是抵抗S的关键受体。金黄色葡萄球菌引起的肺炎，但它有助于肺部的炎症反应。有趣的是，NOD 2的缺乏导致炎症减轻，最终有利于动物恢复。(C)2010年Elsevier Masson SAS。All rights reserved.
Staphylococcus aureus is the most commonly found Gram-positive bacterium in patients admitted in intensive-care units, causing septicaemia or pneumonia. In this work, we investigated the role of NOD2 in S. aureus-induced pneumonia. We found that the absence of NOD2 affected weight loss and recovery speed. Nod2-/- mice showed a reduced lung inflammation in comparison to wild-type animals, with lower presence of cytokines in broncho-alveolar lavage fluids and reduced recruitment of neutrophils. Furthermore, histological analysis of the lungs revealed less severe lesions in Nod2-/- mice at day 2 and day 7 post-infection. In conclusion, we demonstrated that NOD2 is not a crucial receptor to fight S. aureus-induced pneumonia, but that it contributes to the inflammatory response in the lungs. Interestingly, the absence of NOD2 led to a lesser inflammation and was finally beneficial for the animal recovery. (C) 2010 Elsevier Masson SAS. All rights reserved.