Contribution of NOD2 to lung inflammation during Staphylococcus aureus-induced pneumonia

被引:43
作者
Kapetanovic, Ronan [1 ]
Jouvion, Gregory [2 ]
Fitting, Catherine [1 ]
Parlato, Marianna [1 ]
Blanchet, Charlene [1 ]
Huerre, Michel [2 ]
Cavaillon, Jean-Marc [1 ]
Adib-Conquy, Minou [1 ]
机构
[1] Inst Pasteur, Unite Cytokines & Inflammat, Dept Infect & Epidemiol, F-75015 Paris, France
[2] Inst Pasteur, Unite Rech & Expertise Histotechnol & Pathol, Dept Infect & Epidemiol, F-75015 Paris, France
关键词
Innate immunity; Cytokines; Inflammation; Staphylococcus aureus; Pneumonia; DENDRITIC CELLS; HUMAN MONOCYTES; CUTTING EDGE; RECOGNITION; INFECTION; MICE; BACTERIA; IMMUNITY; TLR2; MACROPHAGES;
D O I
10.1016/j.micinf.2010.05.003
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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.
引用
收藏
页码:759 / 767
页数:9
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