Group A Streptococcus emm3 strains induce early macrophage cell death
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Published on: January 9, 2019
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.
Abstract:
Group A Streptococcus (GAS) infections present high morbidity and mortality rates and consequently remain a significant health problem. The emm3 isolates induce more severe pathologies than all others. In this study, we tested, on a collection of invasive and non-invasive emm3 clinical isolates, whether in that genotype the invasive status of the strains affects the innate immune response. We show that phagocytosis is dependent on the invasiveness of the isolates. Interestingly, all emm3 isolates compromise macrophage integrity, already noticeable 1 h after infection. Inflammatory modulators (IL-6, TNF-α and IFN-β) are nevertheless detected during at least 6 h post-infection. This is a likely consequence of the macrophages not being all infected. The efficient and rapid induction of macrophage death could explain the virulence of the emm3 strains.
Insights
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.
