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

Ronan Kapetanovic1, Gregory Jouvion, Catherine Fitting

  • 1Institut Pasteur, Unité Cytokines & Inflammation, Département Infection et épidémiologie, 28 rue du Dr Roux, F-75015 Paris, France.

Microbes and Infection
|May 25, 2010
PubMed

Insights

NOD2 (nucleotide-binding oligomerization domain-containing protein 2) absence in mice reduced lung inflammation and improved recovery from Staphylococcus aureus pneumonia. This suggests NOD2 contributes to, rather than protects against, pneumonia-induced inflammation.

Area of Science:

  • Immunology
  • Microbiology
  • Pulmonary Medicine

Background:

  • Staphylococcus aureus is a common cause of ICU-acquired infections like pneumonia.
  • The role of NOD2 (nucleotide-binding oligomerization domain-containing protein 2) in S. aureus pneumonia is not fully understood.

Purpose of the Study:

  • To investigate the role of NOD2 in the host response to Staphylococcus aureus-induced pneumonia.

Main Methods:

  • Comparison of wild-type and Nod2-/- mice infected with S. aureus.
  • Analysis of weight loss, recovery, lung inflammation, cytokine levels, neutrophil recruitment, and lung histology.

Main Results:

  • Nod2-/- mice exhibited less weight loss and faster recovery.
  • Reduced lung inflammation, lower cytokine levels in broncho-alveolar lavage fluid, and decreased neutrophil infiltration were observed in Nod2-/- mice.
  • Histological analysis showed less severe lung lesions in Nod2-/- mice.

Conclusions:

  • NOD2 is not essential for fighting S. aureus pneumonia but contributes to the inflammatory response.
  • Absence of NOD2 resulted in diminished lung inflammation and improved animal recovery, indicating a beneficial role in this context.

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