Gardnerella vaginalis and Prevotella bivia Trigger Distinct and Overlapping Phenotypes in a Mouse Model of Bacterial Vaginosis.


Journal

The Journal of infectious diseases
ISSN: 1537-6613
Titre abrégé: J Infect Dis
Pays: United States
ID NLM: 0413675

Informations de publication

Date de publication:
30 08 2019
Historique:
received: 16 08 2018
accepted: 14 01 2019
pubmed: 5 2 2019
medline: 28 5 2020
entrez: 5 2 2019
Statut: ppublish

Résumé

Bacterial vaginosis (BV) is a common imbalance of the vaginal microbiota characterized by overgrowth of diverse Actinobacteria, Firmicutes, and Gram-negative anaerobes. Women with BV are at increased risk of secondary reproductive tract infections and adverse pregnancy outcomes. However, which specific bacteria cause clinical features of BV is unclear. We previously demonstrated that Gardnerella vaginalis could elicit many BV features in mice. In this study, we established a BV model in which we coinfected mice with G. vaginalis and another species commonly found in women with BV: Prevotella bivia. This coinfection model recapitulates several aspects of human BV, including vaginal sialidase activity (a diagnostic BV feature independently associated with adverse outcomes), epithelial exfoliation, and ascending infection. It is notable that G. vaginalis facilitated uterine infection by P. bivia. Taken together, our model provides a framework for advancing our understanding of the role of individual or combinations of BV-associated bacteria in BV pathogenesis.

Sections du résumé

BACKGROUND
Bacterial vaginosis (BV) is a common imbalance of the vaginal microbiota characterized by overgrowth of diverse Actinobacteria, Firmicutes, and Gram-negative anaerobes. Women with BV are at increased risk of secondary reproductive tract infections and adverse pregnancy outcomes. However, which specific bacteria cause clinical features of BV is unclear.
METHODS
We previously demonstrated that Gardnerella vaginalis could elicit many BV features in mice. In this study, we established a BV model in which we coinfected mice with G. vaginalis and another species commonly found in women with BV: Prevotella bivia.
RESULTS
This coinfection model recapitulates several aspects of human BV, including vaginal sialidase activity (a diagnostic BV feature independently associated with adverse outcomes), epithelial exfoliation, and ascending infection. It is notable that G. vaginalis facilitated uterine infection by P. bivia.
CONCLUSIONS
Taken together, our model provides a framework for advancing our understanding of the role of individual or combinations of BV-associated bacteria in BV pathogenesis.

Identifiants

pubmed: 30715405
pii: 5305674
doi: 10.1093/infdis/jiy704
pmc: PMC6736442
doi:

Substances chimiques

RNA, Bacterial 0
RNA, Ribosomal, 16S 0
Neuraminidase EC 3.2.1.18

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1099-1108

Subventions

Organisme : NCRR NIH HHS
ID : C06 RR015502
Pays : United States
Organisme : NIDDK NIH HHS
ID : K01 DK110225
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI114635
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI127554
Pays : United States

Commentaires et corrections

Type : CommentIn

Informations de copyright

© The Author(s) 2019. Published by Oxford University Press for the Infectious Diseases Society of America. All rights reserved. For permissions, e-mail: journals.permissions@oup.com.

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Auteurs

Nicole M Gilbert (NM)

Department of Obstetrics and Gynecology, Rheumatology Division, Washington University School of Medicine, St. Louis, Missouri.
Center or Reproductive Health Sciences, Rheumatology Division, Washington University School of Medicine, St. Louis, Missouri.
Center for Women's Infectious Disease Research, Rheumatology Division, Washington University School of Medicine, St. Louis, Missouri.

Warren G Lewis (WG)

Department of Molecular Microbiology, Rheumatology Division, Washington University School of Medicine, St. Louis, Missouri.
Center for Women's Infectious Disease Research, Rheumatology Division, Washington University School of Medicine, St. Louis, Missouri.

Guocai Li (G)

Department of Molecular Microbiology, Rheumatology Division, Washington University School of Medicine, St. Louis, Missouri.
Center for Women's Infectious Disease Research, Rheumatology Division, Washington University School of Medicine, St. Louis, Missouri.
Yangzhou University College of Medicine, Yangzhou, Jiangsu, People's Republic of China.

Dorothy K Sojka (DK)

Department of Medicine, Rheumatology Division, Washington University School of Medicine, St. Louis, Missouri.

Jean Bernard Lubin (JB)

Department of Molecular Microbiology, Rheumatology Division, Washington University School of Medicine, St. Louis, Missouri.
Center for Women's Infectious Disease Research, Rheumatology Division, Washington University School of Medicine, St. Louis, Missouri.
Department of Biological Sciences, University of Delaware, Newark.

Amanda L Lewis (AL)

Department of Obstetrics and Gynecology, Rheumatology Division, Washington University School of Medicine, St. Louis, Missouri.
Department of Molecular Microbiology, Rheumatology Division, Washington University School of Medicine, St. Louis, Missouri.
Center for Women's Infectious Disease Research, Rheumatology Division, Washington University School of Medicine, St. Louis, Missouri.

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