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Neutrophil degranulation mediates severe lung damage triggered by streptococcal M1 protein

O Soehnlein1, S Oehmcke, X Ma

  • 1Dept of Physiology and Pharmacology, Karolinska Institute, 17177 Stockholm, Sweden. Oliver.Sohnlein@ki.se

The European Respiratory Journal
|March 7, 2008
PubMed

Insights

Streptococcus pyogenes M1 protein triggers neutrophil degranulation, causing acute lung injury. Neutrophil granule proteins, not the M1 protein itself, are responsible for this lung damage.

Area of Science:

  • Immunology
  • Pathology
  • Microbiology

Background:

  • Streptococcus pyogenes M1 serotype is linked to severe conditions like streptococcal toxic shock syndrome and acute lung injury.
  • Neutrophils play a critical role in the immune response but can also contribute to tissue damage.

Purpose of the Study:

  • To investigate the role of neutrophils and their secreted products in M1 protein-induced lung damage.
  • To determine if M1 protein directly causes lung injury or if it acts indirectly via neutrophils.

Main Methods:

  • Neutrophil degranulation was analyzed in whole blood via marker analysis of granule subsets.
  • Lung damage in mice was assessed using histology, electron microscopy, bronchoalveolar lavage fluid analysis, and vascular permeability measurements.
  • Experiments involved mice with intact white blood counts, neutropenic mice, and neutropenic mice receiving neutrophil secretions.

Main Results:

  • M1 protein formed complexes with fibrinogen, leading to neutrophil degranulation.
  • M1 protein injection induced neutrophil accumulation, increased vascular permeability, and acute lung damage in mice.
  • Depleting neutrophils prevented lung injury, which was restored upon reintroduction of neutrophil secretions.

Conclusions:

  • Neutrophil degranulation is a key mechanism in M1 protein-induced lung damage.
  • Neutrophil granule proteins are directly responsible for the acute lung injury caused by Streptococcus pyogenes M1 protein.
  • Targeting neutrophil granule proteins may offer therapeutic strategies for M1-associated lung injury.

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