Journal article
Interleukin-17A Contributes to the Control of Streptococcus pyogenes Colonization and Inflammation of the Female Genital Tract
Scientific reports, v 6(1), pp 26836-26836
31 May 2016
PMID: 27241677
Featured in Collection : UN Sustainable Development Goals @ Drexel
Abstract
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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Details
- Title
- Interleukin-17A Contributes to the Control of Streptococcus pyogenes Colonization and Inflammation of the Female Genital Tract
- Creators
- Alison J Carey - Griffith UniversityJason B Weinberg - University of MichiganSuzanne R Dawid - University of MichiganCarola Venturini - The University of QueenslandAlfred K Lam - Griffith UniversityVictor Nizet - University of MontanaMichael G Caparon - Washington University in St. LouisMark J Walker - The University of QueenslandMichael E Watson - University of Michigan Medical SchoolGlen C Ulett - Griffith University
- Publication Details
- Scientific reports, v 6(1), pp 26836-26836
- Publisher
- Springer Nature
- Grant note
- R01 AI077780 / NIAID NIH HHS K12 HD028820 / NICHD NIH HHS
- Resource Type
- Journal article
- Language
- English
- Academic Unit
- Pediatrics; College of Medicine; Drexel University
- Web of Science ID
- WOS:000376877500001
- Scopus ID
- 2-s2.0-84973355582
- Other Identifier
- 991020099833304721
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- Collaboration types
- Domestic collaboration
- International collaboration
- Web of Science research areas
- Immunology