Trichosporon asahii
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA53225 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| DRR032567_1.fastq.gz | Fastqsanger.gz | |||
| DRR032567_2.fastq.gz | Fastqsanger.gz | |||
| DRR037057_1.fastq.gz | Fastqsanger.gz | |||
| DRR037057_2.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 13 |
Similar Datasets
Project description:NBRP: Genome sequencing of Trichosporon asahii JCM 2466
| PRJDB3696 | ENA
Project description:Antifungal mechanism of allicin against Trichosporon asahii: A Transcriptomic Study
| PRJNA1058157 | ENA
Project description:Persister cells are metabolically inactive dormant cells that lie within microbial biofilms. They are phenotypic variants highly tolerant to antimicrobials and, therefore, associated with recalcitrant infections. In the present study, we investigated if Trichosporon asahii and T. inkin are able to produce persister cells. Trichosporon spp. are ubiquitous fungi, commonly found as commensals of the human skin and gut microbiota, and have been increasingly reported as agents of fungemia in immunocompromised patients. Biofilms derived from clinical strains of T asahii (n=5) and T. inkin (n=7) were formed in flat-bottomed microtiter plates and incubated at 35°C for 48 h, treated with 100 μg/ml amphotericin B (AMB) and incubated at 35°C for additional 24 h. Biofilms were scraped from the wells and persister cells were assayed for susceptibility to AMB. Additionally, we investigated if these persister cells were able to generate new biofilms and studied their ultrastructure and AMB susceptibility. Persister cells were detected in both T asahii and T. inkin biofilms and showed tolerance to high doses of AMB (up to 256 times higher than the minimum inhibitory concentration). Persister cells were able to generate biofilms, however they presented reduced biomass and metabolic activity, and reduced tolerance to AMB, in comparison to biofilm growth control. The present study describes the occurrence of persister cells in Trichosporon spp. and suggests their role in the reduced AMB susceptibility of T. asahii and T. inkin biofilms.
| S-EPMC8100310 | biostudies-literature
Project description:This is the first report of the genome sequence of Trichosporon asahii environmental strain CBS 8904, which was isolated from maize cobs. Comparison of the genome sequence with that of clinical strain CBS 2479 revealed that they have >99% chromosomal and mitochondrial sequence identity, yet CBS 8904 has 368 specific genes. Analysis of clusters of orthologous groups predicted that 3,307 genes belong to 23 functional categories and 703 genes were predicted to have a general function.
| S-EPMC3536292 | biostudies-literature
Project description:Trichosporon asahii is an opportunistic pathogenic fungus that causes severe and sometimes fatal infections in immunocompromised patients. Hog1, a mitogen-activated protein kinase, regulates the stress resistance of some pathogenic fungi, however its role in T. asahii has not been investigated. Here, we demonstrated that the hog1 gene-deficient T. asahii mutant is sensitive to high temperature, cell membrane stress, oxidative stress, and antifungal drugs. Growth of the hog1 gene-deficient T. asahii mutant was delayed at 40 °C. The hog1 gene-deficient T. asahii mutant also exhibited sensitivity to sodium dodecyl sulfate, hydrogen peroxide, menadione, methyl methanesulfonate, UV exposure, and antifungal drugs such as amphotericin B under a glucose-rich condition. Under a glucose-restricted condition, the hog1 gene-deficient mutant exhibited sensitivity to NaCl and KCl. The virulence of the hog1 gene-deficient mutant against silkworms was attenuated. Moreover, the viability of the hog1 gene-deficient mutant decreased in the silkworm hemolymph. These phenotypes were restored by re-introducing the hog1 gene into the gene-deficient mutant. Our findings suggest that Hog1 plays a critical role in regulating cellular stress responses in T. asahii.
| S-EPMC10439922 | biostudies-literature
Project description:Trichosporon colonizes the skin, vagina, gastrointestinal and respiratory tract of humans. Superficial infections are common, while disseminated trichosporonosis is rare, specifically seen among immunocompromised patients and often associated with high mortality. We report a rare case Trichosporon asahii infection in a 78-year-old diabetic, with associated acute interstitial glomerulonephritis. Molecular identification of the isolate was confirmed by sequencing IGS1 region of rDNA. Our study adds to a rather limited literature on renal complications of Trichosporonosis.
| S-EPMC8715133 | biostudies-literature
Project description:Transcriptional profiling of Monocyte-like THP-1 Cells with Trichosporon asahii Infected THP-1 Cells comparing untreated THP-1 cells
2012-11-03 | GSE41983 | GEO
Project description:Trichosporon asahii is an emerging opportunistic pathogen that causes potentially fatal disseminated trichosporonosis. The global prevalence of coronavirus disease 2019 (COVID-19) poses an increasing fungal infection burden caused by T. asahii. Allicin is the main biologically active component with broad-spectrum antimicrobial activity in garlic. In this study, we performed an in-depth analysis of the antifungal characteristics of allicin against T. asahii based on physiological, cytological, and transcriptomic assessments. In vitro, allicin inhibited the growth of T. asahii planktonic cells and biofilm cells significantly. In vivo, allicin improved the mean survival time of mice with systemic trichosporonosis and reduced tissue fungal burden. Electron microscopy observations clearly demonstrated damage to T. asahii cell morphology and ultrastructure caused by allicin. Furthermore, allicin increased intracellular reactive oxygen species (ROS) accumulation, leading to oxidative stress damage in T. asahii cells. Transcriptome analysis showed that allicin treatment disturbed the biosynthesis of cell membrane and cell wall, glucose catabolism, and oxidative stress. The overexpression of multiple antioxidant enzymes and transporters may also place an additional burden on cells, causing them to collapse. Our findings shed new light on the potential of allicin as an alternative treatment strategy for trichosporonosis. IMPORTANCE Systemic infection caused by T. asahii has recently been recognized as an important cause of mortality in hospitalized COVID-19 patients. Invasive trichosporonosis remains a significant challenge for clinicians, due to the limited therapeutic options. The present work suggests that allicin holds great potential as a therapeutic candidate for T. asahii infection. Allicin demonstrated potent in vitro antifungal activity and potential in vivo protective effects. In addition, transcriptome sequencing provided valuable insights into the antifungal effects of allicin.
| S-EPMC10269704 | biostudies-literature
Project description:Trichosporon asahii var. asahii CBS 8904 Genome sequencing and assembly
| PRJNA172216 | ENA