Homo sapiens, Others
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA985140 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR24969000_1.fastq.gz | Fastqsanger.gz | |||
| SRR24969000_2.fastq.gz | Fastqsanger.gz | |||
| SRR24969001_subreads.fastq.gz | Fastqsanger.gz | |||
| SRR24969002_subreads.fastq.gz | Fastqsanger.gz | |||
| SRR24969003_subreads.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 204 |
Similar Datasets
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:The skin epidermis provides a vital barrier for preventing transepidermal water loss (TEWL) and environmental stimuli. However, the molecular mechanisms ensuring barrier integrity remain not fully understood. RORα is a nuclear receptor highly expressed in the epidermis of normal skin. However, its epidermal expression is significantly reduced in the lesions of multiple inflammatory skin diseases. In this study, using mice with epidermis-specific Rora gene deletion (RoraEKO), we have demonstrated the central roles of RORα in stabilizing skin barrier function. Albeit the lack of spontaneous skin lesion or dermatitis, RoraEKO mice exhibited elevated TEWL rate and skin features indicating barrier dysfunction. The histological and lipidomic analysis uncovered low levels of cornified envelope proteins and aberrant ceramide composition in the RoraEKO epidermis, implying disturbed late epidermal differentiation. In parallel, RNA-seq analysis revealed altered transcription levels of gene clusters related to “keratinization” and “lipid metabolism” in RORα deficient epidermis. Importantly, epidermal Rora ablation greatly amplified percutaneous allergic inflammatory responses to oxazolone in a mouse allergic contact dermatitis (ACD) model. Our results substantiated the essence of epidermal RORα in maintaining late keratinocyte differentiation and normal barrier function while suppressing cutaneous inflammation.
2024-10-23 | GSE275323 | GEO
Project description:Evaluate the therapeutic effects of different delivery route of MSC treantment in DNCB induced atopic dermatitis mice model.
2023-05-01 | GSE209517 | GEO
Project description:Evaluate the therapeutic effects of different delivery route of MSC treantment in DNCB induced atopic dermatitis mice model.
2023-05-01 | GSE209704 | GEO
Project description:Essential to terrestrial life is the formation of a competent skin barrier that prevents desiccation and entry by harmful substances. A tightly orchestrated series of cellular changes is required for the proper formation of the epidermal permeability barrier. These changes occur in the context of the commensal skin microbiota. Using germ free mice and antibiotic depletion models, we demonstrate the microbiota is necessary for proper differentiation and repair of the barrier. These effects were mediated by keratinocyte signaling through the aryl hydrocarbon receptor (AHR), a xenobiotic receptor that also regulates epidermal differentiation. Murine skin lacking keratinocyte AHR was more susceptible to infection by S. aureus and increased pathology in a model of atopic dermatitis. Topical colonization with a defined consortium of human skin commensals restored barrier competence in germ free skin and during epicutaneous sensitization; these effects were dependent on keratinocyte AHR. We reveal a fundamental role for the commensal skin microbiota in directing skin barrier formation and repair through the AHR, with far-reaching implications for the numerous skin disorders characterized by disrupted epidermal differentiation and/or barrier competence.
2021-03-31 | GSE162925 | GEO
Project description:D-galactose orally intake ameliorate DNCB-induced atopic dermatitis by modulating microbiota composition and quorum sensing. The increased abundance of bacteroidetes and decreased abundance of firmicutes was confirmed. By D-galactose treatment, Bacteroides population was increased and prevotella, ruminococcus was decreased which is related to atopic dermatitis.
2022-04-29 | E-MTAB-11632 | biostudies-arrayexpress
Project description:Epigenetic regulation of gene expression plays a pivotal role in the orchestration of immune responses and may determine the vigor, quality, or longevity of such responses. Chemical allergens can be divided into two categories: skin sensitizing chemicals associated with allergic contact dermatitis, and chemicals that cause sensitization of the respiratory tract and occupational asthma. In mice these are characterized by different T helper (Th) cell responses. To explore the regulation and maintenance of these divergent responses, mice were exposed to 2,4-dinitrochlorobenzene (DNCB; a contact allergen) or trimellitic anhydride (TMA; a respiratory allergen). DNA from draining lymph nodes was processed for methylated DNA immunoprecipitation (MeDIP) followed by hybridization to a whole-genome DNA promoter array. 6319 differently methylated regions (DMR) were identified following DNCB treatment, while 2178 DMRs were measured following TMA treatment, with approximately half of the TMA DMR common to DNCB. When limited to promoter region-associated DMR, 637 genes were uniquely associated with DNCB induced DMR but only 164 genes were unique to TMA DMR. Promoter-associated DMR unique to either DNCB or TMA were generally hypomethylated whereas DMR common to both allergens tended to be hypermethylated. Pathway analyses highlighted a number of immune related pathways, including chemokine and cytokine signalling. These data demonstrate that chemical allergen exposure results in characteristic patterns of DNA methylation indicative of epigenetic regulation of the allergic response. Comparison of methylation profiles from allergens 2,4-dinitrochlorobenzene (DNCB; a contact allergen) and trimellitic anhydride (TMA; a respiratory allergen) or vehicle acetone:olive oil (AOO).
2014-02-07 | E-GEOD-54768 | biostudies-arrayexpress
Project description:Previously, we reported that a null mutation of the Zdhhc13 gene caused by ethylnitrosourea (ENU) mutagenesis in mice resulted in severe systematic phenotypes with amyloidosis, alopecia, dermatitis and osteoporosis. In this study we continued to delineate the pathological mechanism for the dermatitis phenotype and to explore potential palmitoylation substrates of ZDHHC13, which potentially explain the loss-of-function phenotype of ZDHHC13 in skin. Our data clearly suggested that protein S-palmitoylation of a constellation of skin barrier components by ZDHHC13 is crucial for their protein stability, functions, and overall barrier integrity.
2022-02-25 | PXD002958 | Pride
Project description:Flaky tail mice (FTM) with gene mutations to FLG and TMEM79 are known to spontaneously develop atopic dermatitis (AD)-like dermatitis with age. Interestingly, we have already reported that the spontaneous development of dermatitis exhibits site-specificity, i. e. , the face and neck develop spontaneous dermatitis, while the dorsal flank shows normal skin in old FTM. In fact, transepidermal water loss and stratum corneum (SC) pH increased, SC hydration decreased, and epidermis thickened in the neck, but not in the dorsal flank. The detailed pathogenic mechanisms of such site-specific emergence of dermatitis in FTM remain unclear. To clarify the pathogenesis of site-specificity, we analyzed skin of the neck and flank in old FTM using a microarray.
2018-12-28 | GSE124434 | GEO
Project description:Flaky tail mice (FTM) with gene mutations to FLG and TMEM79 are known to spontaneously develop atopic dermatitis (AD)-like dermatitis with age. Interestingly, we have already reported that the spontaneous development of dermatitis exhibits site-specificity, i. e. , the face and neck develop spontaneous dermatitis, while the dorsal flank shows normal skin in old FTM. In fact, transepidermal water loss and stratum corneum (SC) pH increased, SC hydration decreased, and epidermis thickened in the neck, but not in the dorsal flank. The detailed pathogenic mechanisms of such site-specific emergence of dermatitis in AD remain unclear. To clarify the pathogenesis of site-specificity, we analyzed skin of the neck and flank in old FTM using a microarray.
2018-12-28 | GSE124433 | GEO