These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Vaginal dysbiotic bacteria act as pathobionts of the protozoal pathogen Trichomonas vaginalis.
    Author: Hinderfeld AS, Simoes-Barbosa A.
    Journal: Microb Pathog; 2020 Jan; 138():103820. PubMed ID: 31669328.
    Abstract:
    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.
    [Abstract] [Full Text] [Related] [New Search]