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

Microbes Infect. 2010 Sep;12(10):759-67. doi: 10.1016/j.micinf.2010.05.003. Epub 2010 May 21.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Bronchoalveolar Lavage Fluid / chemistry
  • Cytokines / analysis
  • Cytokines / metabolism
  • Histocytochemistry
  • Humans
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Microscopy
  • Neutrophils / immunology
  • Nod2 Signaling Adaptor Protein / deficiency
  • Nod2 Signaling Adaptor Protein / immunology*
  • Pneumonia / immunology
  • Pneumonia / microbiology
  • Pneumonia / pathology*
  • Pneumonia, Staphylococcal / immunology
  • Pneumonia, Staphylococcal / microbiology
  • Pneumonia, Staphylococcal / pathology*
  • Staphylococcus aureus / pathogenicity*

Substances

  • Cytokines
  • Nod2 Signaling Adaptor Protein
  • Nod2 protein, mouse