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J Infect Dis. 2019 Apr 19. pii: jiz167. doi: 10.1093/infdis/jiz167. [Epub ahead of print]

Necrotizing Soft Tissue Infections S.aureus - but not S.pyogenes- isolates display high rate of internalization and cytotoxicity toward human myoblasts.

Author information

1
CIRI, Centre International de Recherche en Infectiologie, Université de Lyon; Inserm U1111; Ecole Normale Supérieure de Lyon; Université Lyon ; CNRS, UMR; Hospices Civils de Lyon ; Lyon, France.
2
Centre National de Référence des Staphylocoques, Institut des Agents Infectieux, Hospices Civils de Lyon, Lyon, France.
3
NeuroMyoGene Institute, Université de Lyon, CNRS UMR5310, INSERM, Lyon, France.
4
Helmholtz-Zentrum für Infektionsforschung GmbH | Inhoffenstraße | Braunschweig.
5
Northern Ireland Center for Stratified Medicine, Biomedical Sciences Research Institute, Londonderry, UK.
6
Division of HIV, Infectious Diseases, and Global Medicine, Department of Medicine, University of California, San Francisco, California, USA.
7
Center for Infectious Medicine, Karolinska Institutet, Karolinska University Hospital | Alfred Nobels Allé | Huddinge, Sweden.

Abstract

BACKGROUND:

Necrotizing Soft Tissue Infections (NSTIs) caused by group A Streptococcus (GAS) and occasionally by Staphylococcus aureus (SA) frequently involve the deep fascia and often lead to muscle necrosis.

METHODS:

To assess the pathogenicity of GAS and SA for muscles in comparison to keratinocytes, adhesion and invasion of NSTI-GAS and NSTI-SA isolates were assessed on these cells, Bloodstream infections (BSI-SA) and non-invasive coagulase negative Staphylococci (CNS) isolates were used as controls.

RESULTS:

NSTI-SA and BSI-SA exhibited stronger internalization into human keratinocytes and myoblasts than NSTI-GAS or CNS. SA internalization reached over 30% in human myoblasts due to a higher percentage of infected myoblasts (>11%) as compared to keratinocytes (<3%). Higher cytotoxicity for myoblasts of NSTI-SA as compared to BSI-SA, was attributed to higher levels of psm and RNAIII transcripts in NSTI-SA. However, the two groups were not discriminated at the genomic level. The cellular basis of high internalization rate in myoblasts was attributed to higher expression of α5β1 integrin in myoblasts. Major contribution of FnbpAB-integrin α5β1 pathway to internalization was confirmed by isogenic mutants.

CONCLUSION:

Our findings suggest the contribution of SA to NSTI severity by a prominent SA invasiveness in muscle cells, a property not shared by NSTI-GAS isolates.

KEYWORDS:

Staphylococcus aureus; Streptococcus ; muscle cells; necrotizing soft tissue infections; pyogenes

PMID:
31001627
DOI:
10.1093/infdis/jiz167

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