ScRNAseq analysis of EC sensitized mouse skin
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE194254 | GEO | 2022/05/09
REPOSITORIES: GEO
Similar Datasets
Project description:ScRNAseq analysis of EC sensitized mouse skin
| PRJNA800006 | ENA
Project description:Cutaneous exposure to food antigen through impaired skin barrier has been shown to induce epicutaneous sensitization, and thereby cause IgE-mediated food allergy. We examined whether skin barrier impairment deteriorated food allergy symptoms in epicutaneously sensitized mice. To clarify the association between skin inflammation and food allergy symptoms, we analyzed gene expression at skin lesions using a GeneChip.
2017-06-30 | GSE95278 | GEO
Project description:Atopic dermatitis is a multifactorial allergic skin disease in humans and dogs. Genetic predisposition, immunologic hyperreactivity, a defective skin barrier and environmental factors play a role in its pathogenesis. The aim of this study was to analyze gene expression in the skin of dogs sensitized to house dust mite antigens. Skin biopsies were collected from six sensitized and six non-sensitized Beagle dogs from normal, non-treated skin before and six and 24 hours after challenge using skin patches with allergen or saline as a negative control. Transcriptome analysis was performed by the use of DNA microarrays and expression of selected genes was validated by quantitative real-time RT-PCR. Expression data was compared between groups (unpaired design). After 24 hours 597 differentially expressed genes were detected, 361 with higher and 226 with lower mRNA concentration in allergen treated skin of sensitized dogs compared to their saline-treated skin and compared to the control specimens. Functional annotation clustering, pathway-and co-citation analysis showed, that the genes with increased expression were involved in inflammation, wound healing and immune response. In contrast, genes with decreased expression in sensitized dogs were associated with differentiation and barrier function of the skin. As the sensitized dogs did not show differences in the untreated skin compared to controls, inflammation after allergen patch test probably led to a decrease in the expression of genes important for barrier formation. Our results further confirm the similar pathophysiology of human and canine atopic dermatitis and revealed genes previously not known to be involved in canine atopic dermatitis. 60 canine (dog) skin tissue samples; six sensitized and six non-sensitized Beagle dogs; samples collected before (0h), 6h and 24h after challenge with allergen; samples collected from a skin area treated with saline and from an area treated with allergen
2014-09-23 | E-GEOD-58442 | biostudies-arrayexpress
Project description:Atopic dermatitis is a multifactorial allergic skin disease in humans and dogs. Genetic predisposition, immunologic hyperreactivity, a defective skin barrier and environmental factors play a role in its pathogenesis. The aim of this study was to analyze gene expression in the skin of dogs sensitized to house dust mite antigens. Skin biopsies were collected from six sensitized and six non-sensitized Beagle dogs from normal, non-treated skin before and six and 24 hours after challenge using skin patches with allergen or saline as a negative control. Transcriptome analysis was performed by the use of DNA microarrays and expression of selected genes was validated by quantitative real-time RT-PCR. Expression data was compared between groups (unpaired design). After 24 hours 597 differentially expressed genes were detected, 361 with higher and 226 with lower mRNA concentration in allergen treated skin of sensitized dogs compared to their saline-treated skin and compared to the control specimens. Functional annotation clustering, pathway-and co-citation analysis showed, that the genes with increased expression were involved in inflammation, wound healing and immune response. In contrast, genes with decreased expression in sensitized dogs were associated with differentiation and barrier function of the skin. As the sensitized dogs did not show differences in the untreated skin compared to controls, inflammation after allergen patch test probably led to a decrease in the expression of genes important for barrier formation. Our results further confirm the similar pathophysiology of human and canine atopic dermatitis and revealed genes previously not known to be involved in canine atopic dermatitis.
2014-09-23 | GSE58442 | GEO
Project description:Skin inflammation exacerbates food allergy symptoms in epicutaneously sensitized mice
| PRJNA376548 | ENA
Project description:Here we identified two populations of myelinated sensory neurons that display markedly different phenotypes in terms of their action potential characteristics and responses to mechanical stimuli based on their expression of Calcitonin Gene-Related Peptide (CGRP). Myelinated neurons that did not express CGRP responded to mechanical stimuli with significantly larger currents during whole-cell voltage clamp recordings than their CGRP-positive counterparts, regardless of whether these neurons projected to the dorsal hindpaw skin or the gastrocnemius muscle. Importantly, this discrepancy could not be explained by a differential expression of mechanosensitive or mechanically-gated proteins like Stoml3 or Piezo2. Following inflammation of the skin or muscle, myelinated neurons demonstrated a sensitization to mechanical stimuli characterized by increased current amplitudes. Interestingly, myelinated neurons expressing CGRP are sensitized to mechanical stimuli following cutaneous inflammation of the paw, while myelinated neurons that do not express CGRP are sensitized to mechanical stimuli following inflammation of the gastrocnemius muscle. Microarray data was obtained from these populations by first using Fluorescence-Activated Cell Sorting (FACS) to separate the populations of interest. 15 different samples were analyzed, 3 biological replicates for each group (5 groups: saline paw-injected, CFA paw-injected, saline muscle-injected, acid muscle-injected, and CFA muscle-injected). The saline injected groups (paw and muscle) are considered controls.
2015-11-06 | E-GEOD-65613 | biostudies-arrayexpress
Project description:Here we identified two populations of myelinated sensory neurons that display markedly different phenotypes in terms of their action potential characteristics and responses to mechanical stimuli based on their expression of Calcitonin Gene-Related Peptide (CGRP). Myelinated neurons that did not express CGRP responded to mechanical stimuli with significantly larger currents during whole-cell voltage clamp recordings than their CGRP-positive counterparts, regardless of whether these neurons projected to the dorsal hindpaw skin or the gastrocnemius muscle. Importantly, this discrepancy could not be explained by a differential expression of mechanosensitive or mechanically-gated proteins like Stoml3 or Piezo2. Following inflammation of the skin or muscle, myelinated neurons demonstrated a sensitization to mechanical stimuli characterized by increased current amplitudes. Interestingly, myelinated neurons expressing CGRP are sensitized to mechanical stimuli following cutaneous inflammation of the paw, while myelinated neurons that do not express CGRP are sensitized to mechanical stimuli following inflammation of the gastrocnemius muscle. Microarray data was obtained from these populations by first using Fluorescence-Activated Cell Sorting (FACS) to separate the populations of interest.
2015-11-06 | GSE65613 | GEO
Project description:To characterize the inflammatory events occuring during early experimental acute AD lesions, skin biopsies were collected 6, 24, and 48 h after epicutaneous application of Dermatophagoides farinae house dust mites (HDM) to sensitized atopic dogs.
2015-11-02 | GSE74136 | GEO
Project description:The skin reprograms its gene expression during dermatitis. This transcriptome profiling examines dermatitis-associated gene expression changes in the skin of mice epicutaneously treated with the Staphylococcus aureus protease SspA, also known as protease V8, and house dust mite extract (HDM). Treatment with SspA and HDM combination results in skin disease in mice that closely resembles atopic dermatitis. The genes whose expression changes in this dermatitis model include cytokines, chemokines, and other molecular mediators of intercellular communication in inflamed skin.
2025-11-27 | GSE311087 | GEO
Project description:Metal allergies are prime examples of delayed hypersensitivity divided in two phases: sensitization and elicitation. Sensitization occurs upon initial contact with the allergen and leads to activation of skin resident cells and formation of metal-reactive T cells. During the elicitation phase, these T cells mount an immune response causing symptoms such as itchy eczema approximately 72 hours after exposure. Research has identified two main mechanisms involved in the initiation of contact hypersensitivity: direct activation of innate immune receptors such as Toll-like receptor 4 by the respective allergen, and conditional innate immune activation via the NLRP3 inflammasome. Elicitation is dominated by the activity of cytotoxic T cells, but it is unclear if only metal-responsive circulating T cells or also tissue-resident T cells contribute. To identify the relevant cell types and signals mediating human nickel hypersensitivity, we used single-cell RNA sequencing of cells from a donor sensitized to nickel (but not chromium) who was epicutaneously exposed to either diluent or both metals for 8 or 72 hours. Our results suggest that nickel exposure specifically activates certain populations of endothelial cells, suprabasal keratinocytes, and CCR7+ dendritic cells within 8 hours, a response not observed with chromium exposure. Skin resident T cells were not involved in the early hypersensitivity response as their gene expression remained unaltered 8 hours after nickel exposure. However, substantial changes in the cutaneous T cell compartments were observed after 72 hours of nickel exposure, including infiltration of SELL+ central memory T cells, effector Tc cells, TH cells, and Treg cells.
2026-03-16 | GSE245577 | GEO