Project description:Trichomonas vaginalis is an extracellular flagellated protozoan responsible for trichomoniasis, one of the most prevalent non-viral sexually transmitted infections. To persist in the host, T. vaginalis employs sophisticated gene regulation mechanisms to adapt to hostile environmental conditions. Although transcriptional regulation is crucial for this adaptation, the specific molecular mechanisms remain poorly understood. Epigenetic regulation, particularly through histone modifications, has emerged as a key modulator of gene expression. Our previous study demonstrated the role of histone modifications H3K4me3 and H3K27Ac in promoting active transcription. However, the full extent of epigenetic regulation in T. vaginalis remained unclear. In this study, we extend these findings by exploring the repressive role of two additional histone H3 modifications, H3K9me3 and H3K27me3. Genome-wide analysis reveals that these modifications are negatively correlated with gene expression, impacting not only protein-coding genes but also repeat genes and transposable elements. These findings offer new insights into the dual role of histone modifications in both activating and repressing gene expression, providing a more comprehensive understanding of epigenetic regulation in T. vaginalis. This expanded knowledge could inform the development of novel therapeutic strategies targeting the epigenetic machinery of this parasite.
Project description:In this study, we investigated genome-wide transcriptional and epigenetic responses of T. vaginalis to histone deacetylase (HDAC) inhibitors.
Project description:Alistipes putredinis can alleviate DSS-induced colitis in mice, but the mechanism is unknown. The aim of this study was to examine the changes in gene expression in the intestinal tissue of mice with colitis following treatment with Alistipes putredinis by RNA sequencing.
Project description:We investigated the effects of B. breve on T. vaginalis growth, gene expression, and host-pathogen interactions. Transcriptomic analyses were performed to characterize T. vaginalis responses to B. breve.
Project description:We aimed to delineate mechanisms of T. vaginalis resistance using transcriptome profiling of metronidazole (MTZ)-resistant and sensitive T. vaginalis clinical isolates.
Project description:Trichomonas vaginalis is an extracellular flagellated protozoan responsible for trichomoniasis, one of the most prevalent non-viral sexually transmitted infections. To persist in the host, T. vaginalis employs sophisticated gene regulation mechanisms to adapt to hostile environmental conditions. Although transcriptional regulation is crucial for this adaptation, the specific molecular mechanisms remain poorly understood. Epigenetic regulation, particularly through histone modifications, has emerged as a key modulator of gene expression. Our previous study demonstrated the role of histone modifications H3K4me3 and H3K27Ac in promoting active transcription. However, the full extent of epigenetic regulation in T. vaginalis remained unclear. In this study, we extend these findings by exploring the repressive role of two additional histone H3 modifications, H3K9me3 and H3K27me3. Genome-wide analysis reveals that these modifications are negatively correlated with gene expression, impacting not only protein-coding genes but also repeat genes and transposable elements. These findings offer new insights into the dual role of histone modifications in both activating and repressing gene expression, providing a more comprehensive understanding of epigenetic regulation in T. vaginalis. This expanded knowledge could inform the development of novel therapeutic strategies targeting the epigenetic machinery of this parasite.
Project description:An anaerobe-dominant, Lactobacillus-deplete cervicovaginal microbiome is associated with adverse reproductive outcomes. Gardnerella vaginalis, a common cervicovaginal anaerobe, alters cervicovaginal epithelial cell function, resulting in inflammatory immune responses and epithelial barrier breakdown. Specific host-microbial mechanisms inducing this epithelial dysfunction remain unknown. Here we show microbe-specific alterations in cervicovaginal epithelial cell metabolite profiles where G. vaginalis, but not Lactobacillus crispatus, increases polyamine biosynthesis. Pretreatment with polyamines (putrescine, spermidine and spermine) globally shifts G. vaginalis-induced transcriptomic profiles. Alterations in transcripts encoding enzymes responsible for polyamine synthesis and catabolism provides further evidence that G. vaginalis modifies polyamine biosynthesis. Additionally, polyamine-mediated transcriptomic changes include genes related to bacterial defense, inflammation, and epigenetic processes. Polyamines mitigate G. vaginalis-induced inflammatory responses through reduction of cytokines, chemokines, and matrix metalloproteinases. The ability of cervicovaginal metabolites to alter microbe-mediated changes in epithelial cell function suggests that metabolite-microbe interactions are critical mediators of epithelial defense against a Lactobacillus-deplete microbiota.
