{"title":"细菌性阴道病相关微生物群与阴道毛滴虫之间的相互作用调节寄生虫诱导的致病性和宿主免疫反应。","authors":"Shu-Fang Chiu, Ching-Yun Huang, Chien-Yung Chen, Wei-Jane Hsu, Yuan-Ming Yeh, Ya-Wen Shih, Lichieh Julie Chu, Wei-Ning Lin, Kuo-Yang Huang","doi":"10.1186/s13071-025-06996-5","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>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.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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.</p><p><strong>Conclusions: </strong>This study significantly advances our understanding of the complex host-bacteria-parasite interactions in the vaginal ecosystem.</p>","PeriodicalId":19793,"journal":{"name":"Parasites & Vectors","volume":"18 1","pages":"346"},"PeriodicalIF":3.5000,"publicationDate":"2025-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12351803/pdf/","citationCount":"0","resultStr":"{\"title\":\"Interactions between bacterial vaginosis-associated microbiota and Trichomonas vaginalis modulate parasite-induced pathogenicity and host immune responses.\",\"authors\":\"Shu-Fang Chiu, Ching-Yun Huang, Chien-Yung Chen, Wei-Jane Hsu, Yuan-Ming Yeh, Ya-Wen Shih, Lichieh Julie Chu, Wei-Ning Lin, Kuo-Yang Huang\",\"doi\":\"10.1186/s13071-025-06996-5\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>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.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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.</p><p><strong>Conclusions: </strong>This study significantly advances our understanding of the complex host-bacteria-parasite interactions in the vaginal ecosystem.</p>\",\"PeriodicalId\":19793,\"journal\":{\"name\":\"Parasites & Vectors\",\"volume\":\"18 1\",\"pages\":\"346\"},\"PeriodicalIF\":3.5000,\"publicationDate\":\"2025-08-14\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12351803/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Parasites & Vectors\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1186/s13071-025-06996-5\",\"RegionNum\":2,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"PARASITOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Parasites & Vectors","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1186/s13071-025-06996-5","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"PARASITOLOGY","Score":null,"Total":0}
Interactions between bacterial vaginosis-associated microbiota and Trichomonas vaginalis modulate parasite-induced pathogenicity and host immune responses.
Background: 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.
Methods: 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.
Results: 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.
Conclusions: This study significantly advances our understanding of the complex host-bacteria-parasite interactions in the vaginal ecosystem.
期刊介绍：
Parasites & Vectors is an open access, peer-reviewed online journal dealing with the biology of parasites, parasitic diseases, intermediate hosts, vectors and vector-borne pathogens. Manuscripts published in this journal will be available to all worldwide, with no barriers to access, immediately following acceptance. However, authors retain the copyright of their material and may use it, or distribute it, as they wish.
Manuscripts on all aspects of the basic and applied biology of parasites, intermediate hosts, vectors and vector-borne pathogens will be considered. In addition to the traditional and well-established areas of science in these fields, we also aim to provide a vehicle for publication of the rapidly developing resources and technology in parasite, intermediate host and vector genomics and their impacts on biological research. We are able to publish large datasets and extensive results, frequently associated with genomic and post-genomic technologies, which are not readily accommodated in traditional journals. Manuscripts addressing broader issues, for example economics, social sciences and global climate change in relation to parasites, vectors and disease control, are also welcomed.
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