ArticleParasites & vectors2025
Interactions between bacterial vaginosis-associated microbiota and Trichomonas vaginalis modulate parasite-induced pathogenicity and host immune responses.
Article in Parasites & vectors, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Epidemiology and transmission dynamics of Trichomonas vaginalis infection among Iranian women: A framework for targeted public health interventions.Parasitology research · 2026Pooled it
- Chemotaxis and selective interactions ofbioRxiv : the preprint server for biology · 2026Article
- The Role of the Vaginal Microbiome in Gynecological Diseases: Mechanistic Insights and Emerging Interventions.Biology · 2026Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
backgroundTrichomoniasis, 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.
methodsWe 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.
resultsOur 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.
conclusionsThis study significantly advances our understanding of the complex host-bacteria-parasite interactions in the vaginal ecosystem.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.