Ontology highlight
ABSTRACT:
PROVIDER: PRJNA715649 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14016700_1.fastq.gz | Fastqsanger.gz | |||
| SRR14016700_2.fastq.gz | Fastqsanger.gz | |||
| SRR14016800_1.fastq.gz | Fastqsanger.gz | |||
| SRR14016800_2.fastq.gz | Fastqsanger.gz | |||
| SRR14016900_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 1224 |
Similar Datasets
Project description:GNPS - Staphylococcus aureus SA113 - Mice atopic dermatitis experiments and culture of SA113
2019-03-16 | MSV000083584 | GNPS
Project description:Expressed on epidermal Langerhans cells, CD1a presents a range of self-lipid antigens found within the skin. However, the extent to which CD1a presents microbial ligands from skin bacteria is unclear. Here, we identified CD1a-dependent T cell responses to phosphatidylglycerol (PG), a ubiquitous bacterial membrane phospholipid, as well as to lysyl phosphatidylglycerol (lysylPG), a modified PG, present in the many gram positive bacteria, and highly abundant in Staphylococcus aureus. Specifically, PG and lysylPG together constitute the vast majority of the structural membrane lipids in Staphylococcus aureus. The crystal structure of the CD1a-lysylPG complex showed that the acyl chains were buried within the A′- and F′-pockets of CD1a, while the lysine-modified phosphoglycerol headgroup protruded from the F′-portal and was available for T cell receptor contact. Using lysylPG-loaded CD1a tetramers, we identified T cells in peripheral blood and in skin that respond to this lipid in a dose dependent manner. Tetramer+ CD4+ T cell lines secreted Th2 cytokines in response to lysylPG as well as to co-cultures of CD1a+ dendritic cells and Staphylococcus aureus. The expansion of CD4+ CD1a-lysylPG tetramer+ T cells in atopic dermatitis patients, indicates a response to a lipid made by bacteria associated with atopic dermatitis, and provide a link supporting involvement of PG-based lipid-specific T cells in the pathogenesis of dermatitis.
2022-12-19 | GSE186459 | GEO
Project description:Atopic dermatitis (AD) is the most common inflammatory skin disease. Stat3 mutation is a major cause of hyper IgE syndrome (HIES), which consistently represent AD like eczematous dermatitis. Based on multi-dimensional transcriptome analysis in pre- and post-flares skin, dermatitis phenotype was controlled by sequential two steps of Stat3 deficiency and environmental pathogenic stimuli. The Stat3 deficiency determined the barrier integrity that lowered threshold of inflammation, but this step was not sufficient to form pathogenicity. Transcriptome data indicated that emergence of dermatitis phenotype need to trigger robust activation of NFB pathway and TH2 cells. Continuous colonization of Staphylococcus aureus was an environmental stimulus to lower the activation threshold of TH2 inflammation in the skin.
2021-10-12 | GSE185340 | GEO
Project description:Skin colonisation of varied communities of commensal microorganisms, such as Staphylococcus aureus (SA), Staphylococcus epidermidis (SE) and Staphylococcus capitis (SC) form the microbiome; a necessity for healthy skin. The skin changes characteristic of atopic dermatitis, a common inflammatory skin disease, have been shown to provide a favourable niche for SA colonisation. We utilised a reconstructed human epidermal (RHE) model recapitulating the stratified anatomy of the epidermis on which to test host responses to bacterial colonisation. SA proliferation was significantly inhibited in contrast to that seen with SE at both high and low colonisation loads after 24 hours. These data strongly suggest species specific regulation of staphylococcal growth, which is partially mediated by interaction with the epidermis.
2023-01-16 | GSE192454 | GEO
Project description:A Pseudomonas aeruginosa-derived neutral ceramidase (PaCDase) isolated from a patient with atopic dermatitis was shown to effectively degrade ceramide in the presence of Staphylococcus aureus-derived lipids or neutral detergents. To understand the effect of ceramide metabolites on the functions of differentiating keratinocytes, we have conducted genes expressions analysis from PaCDase-, sphingosine-1-phosphate (S1P)-treated or untreated three-dimensionally cultured human primary keratinocytes, which form a stratum corneum, in the presence of Triton X-100 using high resolution DNA microarray.
2014-12-25 | GSE53670 | GEO
Project description:Staphylococcus aureus genome sequencing and assembly: atopic dermatitis
| PRJNA511152 | ENA
Project description:<p>The NIH Intramural Skin Microbiome Consortium (NISMC) is a collaboration of investigators with primary expertise in genomics, bioinformatics, large-scale DNA sequencing, dermatology, immunology, allergy, infectious disease, and clinical microbiology. Atopic dermatitis (AD, "eczema") is a chronic relapsing skin disorder that affects ~15% of U.S. children and is associated with $1 billion of medical costs annually. AD is characterized by dry, itchy skin, infiltrated with immune cells. Colonization by Staphylococcus aureus (S. aureus) is ten-fold more common in AD patients and is associated with disease flares. We hypothesize that, in addition to S. aureus, AD may also be associated with additional novel microbes and/or selective shifts of commensal microbes that are relevant to disease progression. The NISMC seeks to define the microbiota that resides in and on the skin and nares of three patient groups, all of whom have eczematous lesions and are currently seen at the NIH Clinical Center: (1) AD patients; (2) Wiskott-Aldrich syndrome (WAS) patients; and (3) Hyper IgE syndrome (HIES) syndrome patients. Examination of the microbiome of patients with WAS or HIES syndromes, both rare immunodeficiencies, will advance our understanding of how an individual's immune system shapes their cutaneous microbial community. We are performing a prospective longitudinal study that follows these groups of patient thorough the cycles of eczema flares, ascertaining clinical data and samples at each stage.</p>
| phs000266 | dbGaP