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Host Response and Inflammation | Spotlight

Differential Induction of Type I and III Interferons by Staphylococcus aureus

Adeline Peignier, Paul J. Planet, Dane Parker
Victor J. Torres, Editor
Adeline Peignier
aDepartment of Pathology, Immunology and Laboratory Medicine, Center for Immunity and Inflammation, Rutgers New Jersey Medical School, Newark, New Jersey, USA
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Paul J. Planet
bDivision of Pediatric Infectious Diseases, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, USA
cDepartment of Pediatrics, Perelman College of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA
dSackler Institute for Comparative Genomics, American Museum of Natural History, New York, New York, USA
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Dane Parker
aDepartment of Pathology, Immunology and Laboratory Medicine, Center for Immunity and Inflammation, Rutgers New Jersey Medical School, Newark, New Jersey, USA
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Victor J. Torres
New York University School of Medicine
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DOI: 10.1128/IAI.00352-20
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ABSTRACT

Staphylococcus aureus is a leading cause of bacterial pneumonia, and we have shown previously that type I interferon (IFN) contributes to the pathogenesis of this disease. In this study, we screened 75 S. aureus strains for their ability to induce type I and III IFN. Both cytokine pathways were differentially stimulated by various S. aureus strains independently of their isolation sites or methicillin resistance profiles. These induction patterns persisted over time, and type I and III IFN generation differentially correlated with tumor necrosis factor alpha production. Investigation of one isolate, strain 126, showed a significant defect in type I IFN induction that persisted over several time points. The lack of induction was not due to differential phagocytosis, subcellular location, or changes in endosomal acidification. A correlation between reduced type I IFN induction levels and decreased autolysis and lysostaphin sensitivity was found between strains. Strain 126 had a decreased rate of autolysis and increased resistance to lysostaphin degradation and host cell-mediated killing. This strain displayed decreased virulence in a murine model of acute pneumonia compared to USA300 (current epidemic strain and commonly used in research) and had reduced capacity to induce multiple cytokines. We observed this isolate to be a vancomycin-intermediate S. aureus (VISA) strain, and reduced Ifnb was observed with a defined mutation in walK that induces a VISA phenotype. Overall, this study demonstrates the heterogeneity of IFN induction by S. aureus and uncovered an interesting property of a VISA strain in its inability to induce type I IFN production.

FOOTNOTES

    • Received 14 June 2020.
    • Returned for modification 6 July 2020.
    • Accepted 13 July 2020.
    • Accepted manuscript posted online 20 July 2020.
  • Supplemental material is available online only.

  • Copyright © 2020 American Society for Microbiology.

All Rights Reserved.

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Differential Induction of Type I and III Interferons by Staphylococcus aureus
Adeline Peignier, Paul J. Planet, Dane Parker
Infection and Immunity Sep 2020, 88 (10) e00352-20; DOI: 10.1128/IAI.00352-20

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Differential Induction of Type I and III Interferons by Staphylococcus aureus
Adeline Peignier, Paul J. Planet, Dane Parker
Infection and Immunity Sep 2020, 88 (10) e00352-20; DOI: 10.1128/IAI.00352-20
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KEYWORDS

Staphylococcus aureus
pneumonia
lung
host-pathogen interactions
type I interferon
type III interferon
VISA
vancomycin

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