UV and skin microbiome
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB65006 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The role of the skin microbiome in UV-induced immune suppression has been overlooked. We addressed the question of microbial involvement in UV-induced immune suppression by using the standard model of contact hypersensitivity in the presence or absence of the microbiome (in germ-free [GF] and disinfected mice) and found that the microbiome inhibits UV-induced immune suppression. Furthermore, our transcriptome analysis (24 hours after irradiation) showed differential regulation of many genes in the presence or absence of the microbiome, including a predominance of pro-inflammatory cytokines versus immunosuppressive cytokines
2019-05-26 | GSE117359 | GEO
Project description:The skin Microbiome stratifies Patients with CTCL into two subgroups. One subgroup has a balanced microbiome, while the other subgroups has a skin dybiosis with S. aureus outgrow. This is accompanied by impaired TCR repertoir and poor clinical outcome.
2023-12-01 | GSE221149 | GEO
Project description:UV-induced CPDs were mapped in primary skin melanocytes or normal human skin fibroblasts following either UVC or UVB irradiation and in isolated human genomic DNA (naked DNA control) that was UVB or UVC irradiated. CPDs were mapped across the human genome using the CPD-capture-seq method and the resulting libraries were captured for ~4000 genomic regions of interest (~3 Mbp) of the human genome by the company Rapid Genomics prior to Illumina sequencing
2023-04-12 | GSE225362 | GEO
Project description:Skin pigmentation is paused following sun exposure, however the mechanism behind this pausing is unknown. Here we found that the UVB-induced DNA repair system, led by the ATM protein kinase, represses MITF transcriptional activity of pigmentation genes while placing MITF in DNA repair mode, thus directly inhibiting pigment production. Phosphoproteomics analysis revealed ATM to be the most significantly enriched pathway among all UVB-induced DNA repair systems. ATM inhibition in mouse or human skin, either genetically or chemically, induces pigmentation. Upon UVB, MITF transcriptional activation is blocked due to ATM dependent phosphorylation of MITF on S414, which modifies MITF activity and interactome towards DNA repair including binding to TRIM28 and RBBP4. Accordingly, MITF genome-occupancy is enriched in sites of high DNA damage that are likely repaired. This suggests that ATM harnesses the pigmentation key activator, for the necessary rapid, efficient DNA repair, thus optimizing the chances of the cell to survive.
2023-07-19 | PXD041121 | Pride
Project description:Modulatory role of skin microbiome against UV
| PRJNA481877 | ENA
Project description:Ultraviolet (UV) light affects endocrinological and behavioral aspects of human sexuality via an unknown mechanism. Using a unique male-female comparative approach, we discovered that the sexual behavioral and hormonal features enhanced by UVB are mediated by the skin. In mice, UV exposure increases hypothalamus-pituitary-gonadal axis hormone levels, resulting in enhanced ovary size, extended estrus days, and anti-Mullerian hormone (AMH) expression. It likewise enhances the sexual responsiveness and attractiveness of females and male-female interactions of both males and females. Conditional knockout of p53 specifically in skin keratinocytes abolished UV’s effects. In humans, UV exposure enhanced romantic passion in both genders increased testosterone levels in men. Our data, revealing that UVB triggers a skin-brain-gonadal axis through skin p53 activation, offers therapeutic opportunities for sex-steroid-related dysfunctions. We speculate that during human furless skin evolution, the skin became the front-line regulator of the response to UVB.
2022-02-17 | PXD025973 | Pride
Project description:In this study, we conducted an integrated analysis of skin measurements, clinical BSTI surveys, and the skin microbiome of 950 Korean subjects to examine the ideal skin microbiome-biophysical association. By utilizing four skin biophysical parameters, we identified four distinct Korean Skin Cutotypes (KSCs) and categorized the subjects into three aging groups based on their age distribution. We established strong connections between 15 core genera and the four KSC types within the three aging groups, revealing three prominent clusters of the facial skin microbiome. Together with skin microbiome variations, skin tone/elasticity distinguishes aging groups while oiliness/hydration distinguishes individual differences within aging groups. Our study provides prospective reality data for customized skin care based on the microbiome environment of each skin type.
| EGAS00001007334 | EGA
Project description:To test the hypothesis that different mechanisms and/or factors might be involved in physiological pigmentary responses of the skin to different types of UV, we used whole human genome microarrays and immunohistochemical analyses to characterize human skin in situ to examine how melanocyte-specific proteins and paracrine melanogenic factors are regulated by repetitive exposure to suberythemal doses of different types of UV (UVA, UVB or SSR). Six volunteers with skin type II-III were irradiated with SSR, UVA or UVB radiation for 2 weeks (5 times per week, 10 times total) after preliminary determination of their MEDs. Biopsies were taken 3 days after the last irradiation.
2010-08-18 | E-GEOD-21429 | biostudies-arrayexpress
Project description:Ultraviolet (UV) radiation is a major melanoma risk factor, yet underlying mechanisms remain poorly understood. Here we introduce a mouse model permitting fluorescence-aided melanocyte imaging and isolation following in vivo UV irradiation. We use expression profiling to show that activated neonatal skin melanocytes isolated following a melanomagenic UVB dose bear a distinct, persistent interferon-response signature, including genes associated with immunoevasion. UVB-induced melanocyte activation, characterized by aberrant growth and migration, was abolished by antibody-mediated systemic blockade of interferon-gamma (IFN-gamma), but not type-I interferons. IFN-gamma was produced by macrophages recruited to neonatal skin by UVB-induced chemokine receptor Ccr2 ligands. Admixed recruited skin macrophages enhanced transplanted melanoma growth by inhibiting apoptosis; notably, IFN-gamma blockade abolished macrophage-associated melanoma growth and survival. IFN-gamma-producing macrophages were identified in 70% of human melanomas examined. Our data reveal an unanticipated role for IFN-gamma in promoting melanocytic cell survival/immunoevasion, and suggest IFN-gamma-R signaling represents a novel therapeutic melanoma target. Biologic replicates of UVA- and UVB-treated mouse melanocytes, as well as untreated mouse melanocytes and mouse keratinocytes, were used to define melanocyte expression signatures associated with UV treatment.
2011-01-01 | E-GEOD-25164 | biostudies-arrayexpress