Ontology highlight
ABSTRACT:
PROVIDER: PRJNA559867 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR9952780_1.fastq.gz | Fastqsanger.gz | |||
| SRR9952780_2.fastq.gz | Fastqsanger.gz | |||
| SRR9952771_1.fastq.gz | Fastqsanger.gz | |||
| SRR9952771_2.fastq.gz | Fastqsanger.gz | |||
| SRR9952781_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 24 |
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Project description:The cell wall provides a major physical interface between fungal pathogens and their mammalian host. This extracellular armour is critical for fungal cell homeostasis and survival. Yet essential cell wall moieties, such as β-1,3-glucan, are recognised as pathogen-associated molecular patterns (PAMPs) that activate immune-mediated clearance mechanisms. We have reported that the opportunistic human fungal pathogen, Candida albicans, masks β-1,3-glucan following exposure to lactate, hypoxia or iron depletion. However, the precise mechanism(s) by which C. albicans masks β-1,3-glucan have remained obscure. Here, we performed proteomic analysis of supernatants harvested from C. albicans cells grown in hypoxia or lactate compared to glucose-grown controls to identify mechanisms driving β-1,3-glucan masking.
2020-06-15 | PXD018044 | Pride
Project description:The cell wall provides a major physical interface between fungal pathogens and their mammalian host. This extracellular armour is critical for fungal cell homeostasis and survival. Yet essential cell wall moieties, such as β-1,3-glucan, are recognised as pathogen-associated molecular patterns (PAMPs) that activate immune-mediated clearance mechanisms. We have reported that the opportunistic human fungal pathogen, Candida albicans, masks β-1,3-glucan following exposure to lactate, hypoxia or iron depletion. However, the precise mechanism(s) by which C. albicans masks β-1,3-glucan have remained obscure. Here, we performed proteomic analysis of cell walls from C. albicans cells grown in hypoxia or lactate compared to glucose-grown controls to identify mechanisms driving β-1,3-glucan masking.
2020-06-15 | PXD018027 | Pride
Project description:RNA sequencing was performed on Candida albicans clinical isolates that display normal (isolates: 3560, 3605, 3609, 4108, 4259) or aberrant (isolates: 3534, 3544, 3621, 3636, 4036) beta-glucan masking in response to lactate and hypoxia. Each clinical isolate was grown to exponential phase in GYNB under normoxic conditions and then exposed for 5 h to: (a) 1% lactate; (b) 0% lactate control; (c) hypoxia; or (d) normoxic control. Three independent experiments were performed for each clinical isolate.
2023-09-05 | E-MTAB-10986 | biostudies-arrayexpress
Project description:Non-specific protective effects against reinfection have been described following infection with Candida albicans. Here we show that mice defective in functional T and B lymphocytes were protected against reinfection with C. albicans in a monocyte-dependent manner. C. albicans and beta glucans induced functional programming of monocytes, leading to enhanced cytokine production in vivo and in vitro. The training required the beta glucan receptor dectin 1 and the non-canonical Raf 1 pathway. Monocyte training by beta-glucans was mediated by epigenetic mechanisms through genome-wide changes in histone trimethylation at H3K4. Pathway analysis showed specific induction of epigenetic changes in genes of innate immunity. The functional programming of monocytes, reminiscent of similar properties of NK cells, has been termed M-bM-^@M-^\trained immunityM-bM-^@M-^] and may be employed for the design of improved vaccination strategies. Chromatin-IP at day7 followed by highthroughput sequencing to look at the differences in H3K4me3 and H3K27me3 binding in Monocytes either cultured in RPMI only versus those trained for 24hrs with beta glucan. Additionally expression analysis was performed by doing strandspecific RNAseq also for both unstimulated and beta glucan trained monocytes for correlating the histone modification changes with the expression changes. Biological replicates were generated from independent samples for H3K4me3 and RNAseq. Additional H3K4me3 ChIP-seq assays were performed for day0 untreated, 24hrs control and beta glucan trained monocytes. H3K4me3 ChIP-seq was also performed for Mouse macrophages both saline(control) and low dose Candida treated.
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Project description:We performed DNA microarray analyses and compared the difference in the transcriptome between B6 and DBA/2 mice with modest or dramatic sensitivity to CAWS-vasculitis, respectively. Candida albicans water-soluble fraction (CAWS), a mannoprotein-β-glucan complex obtained from the culture supernatant of C. albicans NBRC1385, causes CAWS mediated vasculitis (CAWS-vasculitis) with distinct sensitivity among mouse strains.
2013-09-30 | GSE44803 | GEO
Project description:Non-specific protective effects against reinfection have been described following infection with Candida albicans. Here we show that mice defective in functional T and B lymphocytes were protected against reinfection with C. albicans in a monocyte-dependent manner. C. albicans and beta glucans induced functional programming of monocytes, leading to enhanced cytokine production in vivo and in vitro. The training required the beta glucan receptor dectin 1 and the non-canonical Raf 1 pathway. Monocyte training by beta-glucans was mediated by epigenetic mechanisms through genome-wide changes in histone trimethylation at H3K4. Pathway analysis showed specific induction of epigenetic changes in genes of innate immunity. The functional programming of monocytes, reminiscent of similar properties of NK cells, has been termed “trained immunity” and may be employed for the design of improved vaccination strategies.
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Project description:Lactate- and hypoxia-induced beta-glucan masking in responding and non-responding Candida albicans clinical isolates
| PRJEB47705 | ENA
Project description:Galleria mellonella larvae were administered an inoculum of Candida albicans and the cellular and proteomic response to infection over the first 24 hours was monitored. The yeast cell density in infected larvae declined initially but replication commenced six hours post-infection. The hemocyte density decreased from 5.2 × 106/ml to 2.5 × 106/ml at 2 hours but increased to 4.2 × 106 at 6 hours but decreased subsequently. Administration of β - glucan to larvae also resulted in an increase in hemocyte density (5.1 ± 0.22 × 106/ml to 6.25 ± 0.25 × 106/ml, p < 0.05) and the population showed an increase in the density of small, granular type cells at 24 hours (p < 0.05). Hemocytes from larvae inoculated with β - glucan showed faster killing of C. albicans cells (53 ± 4.1% (p < 0.01), 64 ± 3.7%, (p < 0.01), respectively) than hemocytes from control larvae (24 ± 11%) at 60 min. Proteomic analysis indicated increased abundance of immune related proteins cecropin-A (5 fold) and prophenoloxidase-activating proteinase-1 (5 fold) 6 hours post infection but by 24 hours there was elevated abundance of muscle (tropomyosin 2 (141 fold), calponin (66 fold), troponin I (62 fold), troponin T (61 fold)) and proteins indicative of cellular stress (glutathione-S-transferase-like protein (114 fold)), fungal dissemination (muscle protein 20-like protein (174 fold)) and tissue breakdown (mitochondrial cytochrome c (10 fold)). Proteins decreased in abundance at 24 hour included β - 1,3 - glucan recognition protein precursor (29 fold), prophenoloxidase subunit 2 (25 fold) and lysozyme-like protein 1 (5 fold). By characterizing the early responses to infection, G. mellonella larvae may be used to model the initial stages of infection processes in mammals.
2017-09-06 | PXD006879 | Pride
Project description:Extracellular vesicles play an important role in human cellular communication. Here, we show that human and mouse monocytes release TGF-β1-transporting vesicles in response to the pathogenic fungus Candida albicans. Soluble beta-glucan from Candida albicans binds to complement receptor 3 (CR3, CD11b/CD18) on monocytes and induces the release of TGF-β1-transporting vesicles. CR3-dependence is demonstrated using CR3-deficient (CD11b knockout) monocytes generated by CRISPR-CAS9 genome editing and isolated from CR3-deficient (CD11b knockout) mice. Isolated vesicles dampen the pro-inflammatory response in human M1-macrophages as well as in whole blood. Binding of the vesicle-transported TGF-β1 to the TGF-β receptor inhibits IL-1β gene transcription via the SMAD7 pathway in whole blood and induces TGF-β1 transcription in endothelial cells. Inhibition of TGF-β1 relieved the suppression of such proinflammatory effect. Notably, human opsonized apoptotic bodies induce similar TGF-β1-transporting vesicles in monocytes, suggesting that the early immune response is suppressed through this newly identified CR3-dependent anti-inflammatory vesicle pathway.
2020-04-22 | PXD015780 | Pride
Project description:Fungal group III histidine kinases are the molecular targets of some classes of fungicides. In contrast to the yeast Saccharomyces cerevisiae, the fungal pathogen Candida albicans possesses a group III histidine kinase, CaNik1p, also called Cos1p. To investigate the function of CaNIK1, the gene was expressed in S. cerevisiae. The transformants became susceptible to antifungal compounds to which the wild-type strain is resistant. The susceptibility was related to the activation of the MAP kinase Hog1p of the osmotic stress response pathway. Gene expression analysis revealed a strong overlap of the responses to osmotic stress and to fludioxonil at early time points. While the response to fludioxonil persisted, the response to osmotic stress was diminished with time. S. cerevisiae expressing Candida albicans Nik1p were treated with 10 µg/ml fludioxonil. As a comparison, another culture of S. cerevisiae expressing Candida albicans Nik1p was treated with 1 M sorbitol to induce osmotic stress response. One culture remained untreated as a control. From all cultures, samples were taken after a duration of 15, 30 and 60 min.
2014-02-01 | E-GEOD-25002 | biostudies-arrayexpress