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Group A Streptococcus emm3 strains induce early macrophage cell death
Márcia Dinis1, Céline Plainvert2, Magalie Longo1
1INSERM U 1016, Institut Cochin, Unité FRM 'Barrières et Pathogènes' F-75014 Paris, France CNRS UMR 8104, F-75014 Paris, France Université Paris Descartes, Sorbonne Paris Cité, F-75014 Paris, France.
Pathogens and Disease
|December 26, 2015
Summary
Group A Streptococcus (GAS) emm3 strains cause severe infections. Invasive GAS emm3 isolates are phagocytosed differently and rapidly kill macrophages, contributing to their high virulence.
Area of Science:
- Microbiology
- Immunology
- Infectious Diseases
Background:
- Group A Streptococcus (GAS) infections cause significant morbidity and mortality.
- The emm3 genotype of GAS is associated with more severe pathologies compared to other genotypes.
Purpose of the Study:
- To investigate if the invasive status of emm3 GAS clinical isolates influences the innate immune response.
- To understand the interaction between emm3 GAS and macrophages.
Main Methods:
- Testing invasive and non-invasive emm3 GAS clinical isolates.
- Assessing phagocytosis of GAS by macrophages.
- Monitoring macrophage integrity and inflammatory mediator release (IL-6, TNF-α, IFN-β) post-infection.
Main Results:
- Phagocytosis efficiency varied depending on the invasiveness of the emm3 GAS isolates.
- All emm3 GAS isolates compromised macrophage integrity within 1 hour of infection.
- Inflammatory modulators were detected for at least 6 hours, likely due to incomplete macrophage infection.
- Rapid induction of macrophage death was observed.
Conclusions:
- The invasive status of emm3 GAS strains impacts the innate immune response, specifically phagocytosis.
- emm3 GAS efficiently induces rapid macrophage death, which may explain its high virulence.
- Understanding these interactions is crucial for developing effective treatments against severe GAS infections.
