Candida albicans
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ABSTRACT:
PROVIDER: PRJNA241069 | ENA |
REPOSITORIES: ENA
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Project description:Recent cumulative data shows that various transcription factors are recruited to the chromatin in an iron-responsive manner to affect diverse cellular functions in the pathogenic fungus Candida albicans. Here, we identified groups of iron-responsive genes in C. albicans by chromatin remodeling analysis at gene promoters, using micrococcal nuclease (MNase) digestion followed by deep sequencing. Chromatin in the promoter regions of iron uptake and utilization genes showed repressed and active configuration, respectively, under iron-replete conditions. GO Term enrichment analysis of genes with differentially remodeled chromatin, in respective promoter locales, suggested that many genes involved in adhesion are also iron-responsive. C. albicans was observed to be more self-adherent (2-fold increase) and formed higher biofilm mass (77% increase) in the presence of iron. Furthermore, we identified various known and novel adhesion-related genes with iron-dependent active chromatin profiles that are indicative of potential up-regulation under iron-replete conditions. Transcription factor Cph1 that is activated upon Cek1 phosphorylation also showed an active chromatin profile under iron-replete conditions and cells showed iron-responsive Cek1 MAPK phosphorylation in the presence of iron. Thus, iron affects diverse biological functions by modulating chromatin profiles of large gene sets and by signaling through Cek1 MAPK in C. albicans.
2014-11-10 | GSE55819 | GEO
Project description:Candida albicans, the causative agent of mucosal infections including oropharyngeal candidiasis (OPC) as well as bloodstream infections is becoming increasingly resistant to existing treatment options. In the absence of novel drug candidates, drug repurposing aimed at using existing drugs to treat off label diseases is a promising strategy. C. albicans requires environmental iron for survival and virulence while host nutritional immunity deploys iron-binding proteins to sequester iron and reduce fungal growth. Here we evaluated the role of iron-limitation using Deferasirox (an FDA approved iron chelator for treatment of patients with iron overload) during murine OPC; and assessed Deferasirox-treated C. albicans for its interaction with human oral epithelial (OE), neutrophils, and antimicrobial peptides. Therapeutic Deferasirox treatment significantly reduced salivary iron levels while a non-significant reduction in fungal burden was observed. Preventive treatment that allowed for two additional days of drug administration in our murine model, resulted in significant reduction of C. albicans colony forming units (CFU)/g of tongue tissue, a significant reduction in salivary iron levels, and significantly reduced neutrophil-mediated inflammation. C. albicans harvested from tongues of animals undergoing preventive treatment had differential expression of 106 genes, including those involved in iron metabolism, adhesion, and response to host innate immunity. Moreover, Deferasirox-treated C. albicans cells had two-fold reduction in survival in neutrophil phagosomes (with greater susceptibility to oxidative stress); and reduced adhesion and invasion of OE cells, in vitro. Thus Deferasirox treatment has the potential to alleviate OPC by affecting C. albicans gene expression and reducing virulence
2018-12-04 | GSE123277 | GEO
Project description:Transcriptome profiling to identify Cap2/Hap43 regulons in the human fungal pathogen Candida albicans: Wild type vs. cap2D grown in iron-depleted medium
2011-05-25 | GSE28429 | GEO
Project description:C.albicans induces the upregulation of inflammation related genes at the same time it also induces TGF-ß signalling pathway related genes from human blood derived monocytes. RNA sequencing was prerformed from Candida albicans co-incubated monoyctes from 3 different donors. Candida albicans significantly upregulates 6363 genes in human blood derived monocytes in 1h of co-incubation.
2019-10-11 | GSE138681 | GEO
Project description:To characterize the interaction of Candida albicans with intestinal epithelial cells (C2BBe1) from early fungal adhesion to invasion (up to 6 h) and the late translocation and damage phase (12 -24 h), we conducted dual RNA-sequencing of C. albicans-infected C2BBe1 cells over a 24 h time course, with sampling at 0 h, 45 min, 3 h, 6 h, 12 h, and 24 h.
2024-02-07 | GSE237496 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE33460: Transcriptional profile of Candida albicans bcr1 knockout. GSE33461: Transcriptional profile of Candida parapsilosis bcr1 knockout. GSE33462: Transcriptional profile of Candida parapsilosis CLIB214 culture in low iron conditions Refer to individual Series
2011-11-05 | E-GEOD-33490 | biostudies-arrayexpress
Project description:Candida albicans is a common commensal on human mucosal surfaces, but can become pathogenic, e.g. if the host is immunocompromised. While neutrophils, macrophages and T cells-driven activation of neutrophils are regarded as major players in the defence against C. albicans, the role of B cells and the protective function of their antibodies are less well characterized. In this study, we show that human serum antibodies are able to enhance the the association of human macrophages with C. albicans cells . Human serum antibodies are also capable of reducing the growth of the fungi as well as inhibiting adhesion to epithelial cells. Furthermore, human serum antibodies impair C. albicans’ invasion into human oral epithelial cells by blocking induced endocytosis and consequently host cell damage. While aspartic proteases secreted by C. albicans were able to cleave human IgG, this process does not appear to affect the protective function of human antibodies in adhesion. Thus, humans are equipped with antiC. albicans antibodies, which can enhance antifungal activities and which can prevent fungal mediated epithelial damage (even in immunocompromised settings).
2022-04-04 | PXD026082 | Pride
Project description:Iron sequestration by host iron-binding proteins is an important mechanism of resistance to microbial infections. Inside oral epithelial cells, iron is stored within the ferritin, and is therefore usually not accessible to pathogenic microbes. We observed that the ferritin concentration within oral epithelial cells was directly related to their susceptibility to damage by the human pathogenic fungus Candida albicans. Thus, we hypothesized that host ferritin may be used as an iron source by this organism. A screen of C. albicans mutants lacking components of each of the three iron acquisition systems revealed that only the reductive pathway is involved in iron utilization from ferritin by this organism. Transcriptional profiling of wild-type and hyphal-defective C. albicans strains suggested that the C. albicans invasin-like protein Als3 plays a role in ferritin binding.
2008-05-20 | GSE11490 | GEO
Project description:The zinc cluster transcription factor Ahr1p directs Mcm1p regulation of Candida albicans adhesion
| PRJNA134433 | ENA