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Host Response and Inflammation | Spotlight

Group A Streptococcus Infection of the Nasopharynx Requires Proinflammatory Signaling through the Interleukin-1 Receptor

Doris L. LaRock, Raedeen Russell, Anders F. Johnson, Shyra Wilde, Christopher N. LaRock
Victor J. Torres, Editor
Doris L. LaRock
aDepartment of Microbiology and Immunology, Emory University School of Medicine, Atlanta, Georgia, USA
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Raedeen Russell
aDepartment of Microbiology and Immunology, Emory University School of Medicine, Atlanta, Georgia, USA
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Anders F. Johnson
bMicrobiology and Molecular Genetics Program, Graduate Division of Biological and Biomedical Sciences, Emory University, Atlanta, Georgia, USA
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Shyra Wilde
bMicrobiology and Molecular Genetics Program, Graduate Division of Biological and Biomedical Sciences, Emory University, Atlanta, Georgia, USA
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Christopher N. LaRock
aDepartment of Microbiology and Immunology, Emory University School of Medicine, Atlanta, Georgia, USA
cDepartment of Medicine, Division of Infectious Disease, Emory University School of Medicine, Atlanta, Georgia, USA
dAntimicrobial Resistance Center, Emory University, Atlanta, Georgia, USA
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Victor J. Torres
New York University School of Medicine
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DOI: 10.1128/IAI.00356-20
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ABSTRACT

Group A Streptococcus (GAS) is the etiologic agent of numerous high-morbidity and high-mortality diseases. Infections are typically highly proinflammatory. During the invasive infection necrotizing fasciitis, this is in part due to the GAS protease SpeB directly activating interleukin-1β (IL-1β) independent of the canonical inflammasome pathway. The upper respiratory tract is the primary site for GAS colonization, infection, and transmission, but the host-pathogen interactions at this site are still largely unknown. We found that in the murine nasopharynx, SpeB enhanced IL-1β-mediated inflammation and the chemotaxis of neutrophils. However, neutrophilic inflammation did not restrict infection and instead promoted GAS replication and disease. Inhibiting IL-1β or depleting neutrophils, which both promote invasive infection, prevented GAS infection of the nasopharynx. Mice pretreated with penicillin became more susceptible to GAS challenge, and this reversed the attenuation from neutralization or depletion of IL-1β, neutrophils, or SpeB. Collectively, our results suggest that SpeB is essential to activate an IL-1β-driven neutrophil response. Unlike during invasive tissue infections, this is beneficial in the upper respiratory tract because it disrupts colonization resistance mediated by the microbiota. This provides experimental evidence that the notable inflammation of strep throat, which presents with significant swelling, pain, and neutrophil influx, is not an ineffectual immune response but rather is a GAS-directed remodeling of this niche for its pathogenic benefit.

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Group A Streptococcus Infection of the Nasopharynx Requires Proinflammatory Signaling through the Interleukin-1 Receptor
Doris L. LaRock, Raedeen Russell, Anders F. Johnson, Shyra Wilde, Christopher N. LaRock
Infection and Immunity Sep 2020, 88 (10) e00356-20; DOI: 10.1128/IAI.00356-20

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Group A Streptococcus Infection of the Nasopharynx Requires Proinflammatory Signaling through the Interleukin-1 Receptor
Doris L. LaRock, Raedeen Russell, Anders F. Johnson, Shyra Wilde, Christopher N. LaRock
Infection and Immunity Sep 2020, 88 (10) e00356-20; DOI: 10.1128/IAI.00356-20
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KEYWORDS

Streptococcus pyogenes
group A Streptococcus
inflammation
neutrophils
pathogenesis
proteases
respiratory pathogens
virulence factors

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