Interactions between bacterial vaginosis-associated microbiota and Trichomonas vaginalis modulate parasite-induced pathogenicity and host immune responses

TL;DR

This study shows how bacteria linked to bacterial vaginosis can increase the harmful effects of a parasitic infection and change immune responses in the vagina.

Contribution

The study reveals that Prevotella bivia enhances Trichomonas vaginalis pathogenicity and host inflammation through specific molecular pathways.

Findings

Prevotella bivia increases Trichomonas vaginalis adhesion and cytotoxicity in host cells.

P. bivia triggers IL-6, IL-8, CXCL1, and IP-10 secretion and activates MAPK pathways in Ect1 cells.

The interaction promotes epithelial-mesenchymal transition, worsening infection outcomes.

Abstract

Trichomoniasis, caused by Trichomonas vaginalis (Tv), is the most common nonviral sexually transmitted infection (STI). Bacterial vaginosis (BV) is characterized by a reduction in health-associated Lactobacillus and an overgrowth of anaerobes. Both BV-associated bacteria (BVB) and Tv are linked to adverse gynecologic outcomes. Herein, we aimed to investigate whether interactions between vaginal bacterial species and Tv could modulate Tv pathogenicity and Tv-induced host immune responses.

We established a co-culture system to evaluate the interaction between Tv and various vaginal bacteria, including Lactobacillus crispatus, Escherichia coli, Prevotella bivia, and Lactobacillus iners, in the context of polymicrobial infection in ectocervical cells (Ect1). The impact of the interactions between Tv and these bacterial species on Tv adhesion, Tv-induced cytotoxicity in Ect1 cells, and cytokine secretion were assessed. Additionally, the molecular mechanisms governing host inflammation following Tv-bacteria interactions were investigated.

Our in vitro model showed that specific BVB, particularly P. bivia, enhanced the expression of Tv ap65 gene and promoted Tv adhesion to host cells. Additionally, Tv pretreated with P. bivia increased cytotoxicity and upregulated IL-6, IL-8, CXCL1, and IP-10 secretion in Ect1 cells. Furthermore, Ect1 cells stimulated with Tv pretreated with P. bivia also activated the PI3K, ERK, and p38 MAPK pathways, triggering epithelial-mesenchymal transition (EMT) events. These results demonstrate that this potential pathobiont enhances Tv pathogenicity, highlighting the impact of the vaginal microbiome on host cells during Tv infection.

This study significantly advances our understanding of the complex host-bacteria-parasite interactions in the vaginal ecosystem.

The online version contains supplementary material available at 10.1186/s13071-025-06996-5.

Figures