Skin metagenome
Ontology highlight
ABSTRACT:
PROVIDER: PRJDB13737 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| DRR383751_1.fastq.gz | Fastqsanger.gz | |||
| DRR383751_2.fastq.gz | Fastqsanger.gz | |||
| DRR383752_1.fastq.gz | Fastqsanger.gz | |||
| DRR383752_2.fastq.gz | Fastqsanger.gz | |||
| DRR383753_1.fastq.gz | Fastqsanger.gz |
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Project description:Monogenic skin disease driven by staphylococcal dysbiosis
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Project description:Dermal macrophages (Macs) are essential for the timely resolution of staphylococcal skin infections. However the cell intrinsic pathways and microenvironmental cues that mediate this are unclear. Here we analyzed a strictly intradermal ear infection model with Staphylococcus aureus (S. aureus) to explore immunometabolic regulation.
2024-05-01 | GSE174675 | GEO
Project description:Dermal macrophages (Macs) are essential for the timely resolution of staphylococcal skin infections. However the cell intrinsic pathways and microenvironmental cues that mediate this are unclear. Here we analyzed a strictly intradermal ear infection model with Staphylococcus aureus (S. aureus) to explore immunometabolic regulation.
2024-05-01 | GSE174674 | GEO
Project description:USA300 Staphylococcus aureus is responsible for the current outbreak of skin abscesses in the United States. Unlike other USA types, USA300 colonizes the rectum at rates higher than the nose. The reason for the difference in colonization site preference may be related to specific adherence or attachment factors contained in the genome of these strains. Additional knowledge in this field may help design novel prophylactic and therapeutic strategies to combat staphylococcal infections. Strains of USA300 MSSA and MRSA colonizing the nose and/or rectum from children with staphylococcal skin abscesses were compared by whole genome array technology to identify bacterial genetic determinants associated with site-specific colonization. Strains isolated from different colonization sites were indistinguishable by genomic content. Site-specific colonization traits were not detected in the colonizing bacteria by this array. Either host characteristics associated with staphylococcal carriage or under represented bacterial genomic constructions need to be examined to determine the etiology of this site-specific colonization. Data is also available from <ahref=http://bugs.sgul.ac.uk/E-BUGS-102 target=_blank>BuG@Sbase</a>
2011-04-15 | E-BUGS-102 | biostudies-arrayexpress
Project description:Type III interferons (IFN-λ) are antiviral and immunomodulatory cytokines that have been best characterized in respiratory and gastrointestinal infections, but the effects of IFN-λ against skin infections have not been extensively investigated. We sought to define the skin-specific effects of IFN-λ against the highly prevalent human pathogen herpes simplex virus (HSV). We infected mice lacking the IFN-λ receptor (Ifnlr1-/-), both the IFN-λ and the IFN-αβ receptor (Ifnar1-/- Ifnlr1-/-), or IFN-λ cytokines (Ifnl2/3-/-) and found that IFN-λ restricts the severity of HSV-1 and HSV-2 skin lesions, independent of a direct effect on viral load. Using conditional knockout mice, we found that IFN-λ signaling in both keratinocytes and neutrophils was necessary to control HSV-1 skin lesion severity, and that IFN-λ signaling in keratinocytes suppressed CXCL9-mediated neutrophil recruitment to the skin. Furthermore, depleting neutrophils prevented the development of severe HSV-1 skin lesions in Ifnlr1-/- mice. Altogether, our results suggest that IFN-λ plays an immunomodulatory role in the skin that restricts neutrophil-mediated pathology during HSV infection, and suggest potential applications for IFN-λ in treating viral skin infections.
2023-09-12 | GSE242170 | GEO
Project description:Type III interferons (IFN-λ) are antiviral and immunomodulatory cytokines that have been best characterized in respiratory and gastrointestinal infections, but the effects of IFN-λ against skin infections have not been extensively investigated. We sought to define the skin-specific effects of IFN-λ against the highly prevalent human pathogen herpes simplex virus (HSV). We infected mice lacking the IFN-λ receptor (Ifnlr1-/-), both the IFN-λ and the IFN-αβ receptor (Ifnar1-/- Ifnlr1-/-), or IFN-λ cytokines (Ifnl2/3-/-) and found that IFN-λ restricts the severity of HSV-1 and HSV-2 skin lesions, independent of a direct effect on viral load. Using conditional knockout mice, we found that IFN-λ signaling in both keratinocytes and neutrophils was necessary to control HSV-1 skin lesion severity, and that IFN-λ signaling in keratinocytes suppressed CXCL9-mediated neutrophil recruitment to the skin. Furthermore, depleting neutrophils prevented the development of severe HSV-1 skin lesions in Ifnlr1-/- mice. Altogether, our results suggest that IFN-λ plays an immunomodulatory role in the skin that restricts neutrophil-mediated pathology during HSV infection, and suggest potential applications for IFN-λ in treating viral skin infections.
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Project description:Atopic dermatitis (AD) is a chronic pruritic inflammatory skin disease. We recently described an animal model in which repeated epicutaneous applications of a house dust mite extract and Staphylococcal enterotoxin B induced eczematous skin lesions. In this study we showed that global gene expression patterns are very similar between human AD skin and allergen/staphylococcal enterotoxin B–induced mouse skin lesions, particularly in the expression of genes related to epidermal growth/differentiation, skin barrier, lipid/energy metabolism, immune response, or extracellular matrix. In this model, mast cells and T cells, but not B cells or eosinophils, were shown to be required for the full expression of dermatitis, as revealed by reduced skin inflammation and reduced serum IgE levels in mice lacking mast cells or T cells (TCRb-/- or Rag1-/-). The clinical severity of dermatitis correlated with the numbers of mast cells, but not eosinophils. Consistent with the idea that T helper type 2 (Th2) cells play a predominant role in allergic diseases, the receptor for the Th2-promoting cytokine thymic stromal lymphopoietin and the high-affinity IgE receptor, FceRI, were required to attain maximal clinical scores. Therefore, this clinically relevant model provides mechanistic insights into the pathogenic mechanism of human AD. A total of six samples were analyzed. Back skin samples from healthy or AD-induced C57BL/6, PLC-beta 3 KO (C57BL/6 background), and NC/Nga mice were collected for total RNA extraction. Pooled RNA from 2-4 mice per condition were used for analysis.
2013-12-10 | E-GEOD-53132 | biostudies-arrayexpress
Project description:Atopic dermatitis (AD) is a chronic pruritic inflammatory skin disease. We recently described an animal model in which repeated epicutaneous applications of a house dust mite extract and Staphylococcal enterotoxin B induced eczematous skin lesions. In this study we showed that global gene expression patterns are very similar between human AD skin and allergen/staphylococcal enterotoxin B–induced mouse skin lesions, particularly in the expression of genes related to epidermal growth/differentiation, skin barrier, lipid/energy metabolism, immune response, or extracellular matrix. In this model, mast cells and T cells, but not B cells or eosinophils, were shown to be required for the full expression of dermatitis, as revealed by reduced skin inflammation and reduced serum IgE levels in mice lacking mast cells or T cells (TCRb-/- or Rag1-/-). The clinical severity of dermatitis correlated with the numbers of mast cells, but not eosinophils. Consistent with the idea that T helper type 2 (Th2) cells play a predominant role in allergic diseases, the receptor for the Th2-promoting cytokine thymic stromal lymphopoietin and the high-affinity IgE receptor, FceRI, were required to attain maximal clinical scores. Therefore, this clinically relevant model provides mechanistic insights into the pathogenic mechanism of human AD.
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Project description:Metabolic rewiring tunes dermal macrophages in staphylococcal skin infection
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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.
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