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ABSTRACT:
PROVIDER: PRJNA863122 | ENA |
REPOSITORIES: ENA
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Project description:RNA-seq analysis of an in vivo murine model of vulvovaginal candidiasis
2015-04-11 | GSE67688 | GEO
Project description:RNA-seq analysis of an in vivo murine model of vulvovaginal candidiasis Murine vaginas were infected with Candida albicans and harvested for RNA-seq analysis 3 days post-infection
2015-04-11 | E-GEOD-67688 | biostudies-arrayexpress
Project description:Problem: Recurrent vulvovaginal candidiasis (RVVC) affects 5-10% of all women, negatively impacting their reproductive health and quality of life. Herein, we investigated the molecular effects of RVVC on the vaginal mucosa of otherwise healthy women. Methods: Gene expression analysis was performed on vaginal tissue biopsies from women with RVVC, including those with a current episode of vulvovaginal candidiasis (RVVC, n=19) and women between infections (CNR, n=8); women asymptomatically colonized with Candida albicans (AS, n=7); and healthy controls (n=18). Gene expression profiles were compared between groups and correlated with clinical data retrieved from questionnaires and gynecologic examinations. Results: Of 20,171 genes identified in vaginal biopsies, 6,506 were differentially expressed in the RVVC group, compared to healthy controls. Gene expression pathway analysis revealed an association between RVVC and pathways of inflammatory responses, especially genes involved in neutrophil recruitment and activation. Expression of genes involved in inflammation and neutrophil recruitment increased with increasing clinical severity of vulvovaginal candidiasis, whereas expression of some genes involved in epithelial integrity decreased with increasing clinical severity of infection. Gene expression profiles of both the CNR and AS groups were comparable to those of healthy controls. Conclusions: The clinical severity of RVVC during active infection correlates with increased expression of genes involved in molecular inflammation and neutrophil activation in the vaginal mucosa. The lack of differences between healthy controls and women with RVVC who were between acute infections indicates that the molecular effects observed in the RVVC group are only present during active infection.
2025-01-15 | GSE278036 | GEO
Project description:Diverse vaginal microbiomes in reproductive-age women with vulvovaginal candidiasis
| PRJEB4606 | ENA
Project description:Recurrent vulvovaginal candidiasis: a dynamic interkingdom biofilm disease of Candida and Lactobacillus
| PRJNA719953 | ENA
Project description:Transcriptomic analysis of vulvovaginal candidiasis identifies a role for the NLRP3 inflammasome
| PRJNA280807 | ENA
Project description:Candida albicans is a commensal of the urogenital tract and the predominant cause of vulvovaginal candidiasis (VVC). Roughly, 70% of otherwise healthy women succumb to VVC at least once in their life time. Elevated oestrogen levels are associated with C. albicans colonisation of the vagina and symptomatic infection. However, little is known about how C. albicans adapts to oestrogen. Here, we investigate how adaptation of C. albicans to elevated concentrations of oestrogen on the C. albicans host-pathogen interaction. Growth of C. albicans in physiological relevant concentrations of oestrogen promoted fungal innate immune evasion through reduction of both macrophage and neutrophil phagocytosis. Oestrogen-induced innate immune evasion was mediated via inhibition of opsonophagocytosis through enhanced Gpd2 dependent acquisition of Factor H on the fungal cell surface. The zebrafish larval model of infection confirmed that in vivo oestrogen and Gpd2 promote pathogenicity. Understanding the impact of oestrogen on C. albicans host-pathogen interaction will help improve our knowledge on how oestrogen promotes VVC.
2022-01-04 | GSE145240 | GEO