Vaginal dysbiotic bacteria act as pathobionts of the protozoal pathogen Trichomonas vaginalis.
Adhesion
Bacterial vaginosis
Biofilm
Gardnerella vaginalis
Trichomonas vaginalis
Trichomoniasis
Vaginal microbiota
Journal
Microbial pathogenesis
ISSN: 1096-1208
Titre abrégé: Microb Pathog
Pays: England
ID NLM: 8606191
Informations de publication
Date de publication:
Jan 2020
Jan 2020
Historique:
received:
27
08
2019
revised:
22
10
2019
accepted:
23
10
2019
pubmed:
2
11
2019
medline:
21
10
2020
entrez:
1
11
2019
Statut:
ppublish
Résumé
Trichomoniasis, a prevalent sexually transmitted infection caused by the protozoan parasite Trichomonas vaginalis, is often accompanied by a vaginal dysbiotic microbiota of pathogenic potential. Our objective was to investigate whether these dysbiotic bacteria act as pathobionts of T. vaginalis infection by altering pathogenic capabilities of the parasite, particularly in regard to adhesion to vaginal substrates and viability of human ectocervical cells. Assays interrogated the performance of T. vaginalis adhesion to biofilm produced by vaginal dysbiotic bacteria and whether these bacteria were capable of altering the ability of the parasite to bind to mucins and cells. The binding activities of T. vaginalis were quantified by flow cytometry. Host cell viability and apoptosis, as affected by T. vaginalis with or without the bacteria, were also measured experimentally. An in vitro biofilm was shown to provide adhesion for T. vaginalis. The binding of parasites to mucins and cells was modulated by the vaginal dysbiotic bacteria. Parasite cytoadhesion was significantly increased by these bacteria. In addition, these bacteria enhanced the pathogenic effects of the parasite to host cells. Together, this study showed that dysbiotic bacteria accompanying T. vaginalis infection in the vagina function as pathobionts as they are capable of enhancing the pathogenic capabilities of this parasite. This study highlights the importance of understanding the contribution of the vaginal microbiome to trichomoniasis.
Identifiants
pubmed: 31669328
pii: S0882-4010(19)31506-2
doi: 10.1016/j.micpath.2019.103820
pii:
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
103820Informations de copyright
Copyright © 2019 Elsevier Ltd. All rights reserved.