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Myeloid-related protein-14 deficiency promotes inflammation in staphylococcal pneumonia

Ahmed Achouiti1, Thomas Vogl2, Anne J Van der Meer3

  • 1Center for Experimental and Molecular Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands Center for Infection and Immunity Amsterdam, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands a.achouiti@amc.nl.

The European Respiratory Journal
|March 21, 2015
PubMed

Insights

Myeloid-related protein (MRP)8/14, typically pro-inflammatory, unexpectedly protects the lungs during Staphylococcus aureus pneumonia. Mice lacking MRP8/14 showed worsened lung inflammation and pathology, indicating a protective role.

Area of Science:

  • Immunology
  • Pulmonary Medicine
  • Microbiology

Background:

  • Staphylococcus aureus is a significant cause of hospital and community-acquired pneumonia.
  • Staphylococcal lung infections can trigger severe pulmonary inflammation.
  • Neutrophils release myeloid-related protein (MRP)8/14 complexes during S. aureus infection, known for pro-inflammatory and chemotactic activities.

Purpose of the Study:

  • To investigate the specific role of MRP8/14 in the host's response to S. aureus pneumonia.
  • To determine if MRP8/14 contributes to bacterial clearance or modulates inflammation during staphylococcal pneumonia.

Main Methods:

  • Pneumonia was induced in wildtype and MRP14-deficient mice via intranasal inoculation of S. aureus USA300.
  • Mice were analyzed at multiple time points (6, 24, 48, 72 hours) post-infection.
  • Levels of MRP8/14, bacterial load, cytokine concentrations, neutrophil transmigration, and lung histopathology were assessed.

Main Results:

  • MRP8/14 levels significantly increased in bronchoalveolar lavage fluid and lung tissue during S. aureus pneumonia.
  • MRP14 deficiency resulted in aggravated lung histopathology and increased cytokine levels.
  • Mice lacking MRP14 exhibited diminished neutrophil transmigration and reduced nucleosome release at later infection stages.
  • Bacterial clearance was only marginally affected by MRP14 deficiency.

Conclusions:

  • MRP8/14 plays an unexpected protective role in the lung during Staphylococcus aureus pneumonia.
  • Despite its known pro-inflammatory properties, MRP8/14 appears to mitigate lung damage and inflammation in this context.
  • Further research is warranted to elucidate the precise mechanisms behind MRP8/14's protective function.

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