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Interleukin-17A Contributes to the Control of Streptococcus pyogenes Colonization and Inflammation of the Female Genital Tract
Journal article   Open access   Peer reviewed

Interleukin-17A Contributes to the Control of Streptococcus pyogenes Colonization and Inflammation of the Female Genital Tract

Alison J Carey, Jason B Weinberg, Suzanne R Dawid, Carola Venturini, Alfred K Lam, Victor Nizet, Michael G Caparon, Mark J Walker, Michael E Watson and Glen C Ulett
Scientific reports, v 6(1), pp 26836-26836
31 May 2016
PMID: 27241677
url
https://www.nature.com/articles/srep26836.pdfView
Published, Version of Record (VoR) Open
url
https://doi.org/10.1038/srep26836View
Published, Version of Record (VoR) Open

Abstract

Animals Female Inflammation - immunology Inflammation - metabolism Inflammation - microbiology Inflammation Mediators - immunology Inflammation Mediators - metabolism Interleukin-17 - immunology Lymphocytes - immunology Mice, Inbred C57BL Mice, Knockout Neutrophil Infiltration Reproductive Tract Infections - immunology Reproductive Tract Infections - metabolism Reproductive Tract Infections - microbiology Streptococcal Infections - immunology Streptococcus pyogenes - immunology Vagina - immunology Vagina - metabolism Vagina - microbiology
Postpartum women are at increased risk of developing puerperal sepsis caused by group A Streptococcus (GAS). Specific GAS serotypes, including M1 and M28, are more commonly associated with puerperal sepsis. However, the mechanisms of GAS genital tract infection are not well understood. We utilized a murine genital tract carriage model to demonstrate that M1 and M28 GAS colonization triggers TNF-α, IL-1β, and IL-17A production in the female genital tract. GAS-induced IL-17A significantly influences streptococcal carriage and alters local inflammatory responses in two genetically distinct inbred strains of mice. An absence of IL-17A or the IL-1 receptor was associated with reduced neutrophil recruitment to the site of infection; and clearance of GAS was significantly attenuated in IL-17A(-/-) mice and Rag1(-/-) mice (that lack mature lymphocytes) but not in mice deficient for the IL-1 receptor. Together, these findings support a role for IL-17A in contributing to the control of streptococcal mucosal colonization and provide new insight into the inflammatory mediators regulating host-pathogen interactions in the female genital tract.

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Collaboration types
Domestic collaboration
International collaboration
Web of Science research areas
Immunology
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