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ABSTRACT:
PROVIDER: PRJNA1199545 | ENA |
REPOSITORIES: ENA
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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:Diverse vaginal microbiomes in reproductive-age women with vulvovaginal candidiasis
| PRJEB4606 | ENA
Project description:RNA-seq analysis of an in vivo murine model of vulvovaginal candidiasis
2015-04-11 | GSE67688 | GEO
Project description:Candida glabrata is a human-associated opportunistic fungal pathogen. It shares its niche with Lactobacillus spp. in the gastrointestinal and vaginal tract. In fact, Lactobacillus species are thought to competitively prevent Candida overgrowth. We investigated the molecular aspects of this antifungal effect by analyzing the interaction of C. glabrata strains with Limosilactobacillus fermentum. From a collection of clinical C. glabrata isolates, we identified strains with different sensitivities to L. fermentum in coculture. We analyzed the variation of their expression pattern to isolate the specific response to L. fermentum. C. glabrata-L. fermentum coculture induced genes associated with ergosterol biosynthesis, weak acid stress, and drug/chemical stress. L. fermentum coculture depleted C. glabrata ergosterol. The reduction of ergosterol was dependent on the Lactobacillus species, even in coculture with different Candida species. We found a similar ergosterol-depleting effect with other lactobacillus strains (Lactobacillus crispatus and Lactobacillus rhamosus) on Candida albicans, Candida tropicalis, and Candida krusei. The addition of ergosterol improved C. glabrata growth in the coculture. Blocking ergosterol synthesis with fluconazole increased the susceptibility against L. fermentum, which was again mitigated by the addition of ergosterol. In accordance, a C. glabrata Derg11 mutant, defective in ergosterol biosynthesis, was highly sensitive to L. fermentum. In conclusion, our analysis indicates an unexpected direct function of ergosterol for C. glabrata proliferation in coculture with L. fermentum.
2023-02-08 | GSE202656 | GEO
Project description:In this study we used a transcriptomic approach to study the molecular determinants of the synergy between copper and fluconazole, in Candida glabrata, the second most frequent cause of invasive candidiasis. We demonstrate that copper acts together with fluconazole by downregulating three distinct pathways: azole efflux, ergosterol biosynthesis and zinc homeostasis. Coincidently, all these pathways are important for C. glabrata to cope with fluconazole stress. Therefore, when copper and fluconazole are combined cells fail to detoxify this drug and accumulate toxic methylated intermediates of sterol metabolism. This accumulation, possibly together with copper-induced lipid damages, should affect the activity of plasma membrane transporters, which impedes zinc uptake, leading to zinc depletion
2022-06-01 | GSE162741 | GEO
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
Project description:Vulvovaginal candidiasis (VVC) affects nearly ¾ of women during their lifetime and its symptoms seriously reduce quality of life. Although Candida albicans is a common commensal, it is unknown if VVC results from a commensal to pathogenic state switch, if only some strains can cause VVC, and/or if there is displacement of commensal strains with more pathogenic strains. We studied a set of VVC and Colonizing C. albicans strains to identify consistent in vitro phenotypes associated with one group or the other. We find that the strains do not differ in overall genetic profile or behavior in culture media (i.e. MLST profile, rate of growth, filamentation), but they show strikingly different behavior during their interactions with vaginal epithelial cells. Epithelial infections with VVC-derived strains yielded stronger fungal proliferation and shedding of fungi and epithelial cells. RNA-seq analysis of representative epithelial cell infections with selected pathogenic or commensal isolates identified several differentially activated epithelial signaling pathways, including the integrin, ferroptosis and type I interferon pathways; the latter has been implicated in damage protection. The type I interferon pathway is activated more by the Colonizing strains, while type I interferon inhibition selectively increases fungal shedding of only the colonizing fungi. These data suggest that VVC strains may intrinsically have more pathogenic potential via differential elicitation of epithelial responses, including type I interferon pathway. Therefore, it may be possible to evaluate pathogenic potential in vitro to refine VVC diagnosis.
2023-02-07 | GSE207081 | GEO
Project description:Recurrent vulvovaginal candidiasis: a dynamic interkingdom biofilm disease of Candida and Lactobacillus
| PRJNA719953 | ENA