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The lectin-like domain of thrombomodulin hampers host defence in pneumococcal pneumonia

Marcel Schouten1, J Daan de Boer, Cornelis van 't Veer

  • 1Center for Experimental and Molecular Medicine,Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.

The European Respiratory Journal
|September 1, 2012
PubMed

Insights

Mice lacking the lectin-like domain of thrombomodulin (TM) showed improved survival and reduced inflammation during Streptococcus pneumoniae infection. This suggests the TM lectin-like domain may worsen severe Gram-positive bacterial pneumonia.

Area of Science:

  • Immunology
  • Microbiology
  • Pathology

Background:

  • The lectin-like domain of thrombomodulin (TM) is crucial in sterile inflammation.
  • Its role in severe Gram-positive bacterial infections, like pneumococcal pneumonia, remains unclear.

Purpose of the Study:

  • To investigate the function of the TM lectin-like domain in a murine model of Streptococcus pneumoniae pneumonia.

Main Methods:

  • Wild-type and TM lectin-like domain-deficient (TM(LeD/LeD)) mice were infected intranasally with S. pneumoniae.
  • Survival rates, bacterial loads, pulmonary inflammation, neutrophil infiltration, and cytokine/chemokine levels were assessed.

Main Results:

  • TM(LeD/LeD) mice exhibited significantly better survival rates compared to wild-type mice.
  • Reduced bacterial loads in blood and liver, attenuated pulmonary inflammation, and lower inflammatory mediator levels were observed in TM(LeD/LeD) mice.
  • Plasma pro-inflammatory cytokine levels were also decreased in TM(LeD/LeD) mice post-infection.

Conclusions:

  • Deletion of the TM lectin-like domain enhances host defense against pneumococcal pneumonia.
  • The TM lectin-like domain might play a differential role in responses to Gram-positive versus Gram-negative bacterial infections.

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