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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Der f/SEB-induced skin inflammation

ABSTRACT: 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.

ORGANISM(S): Mus musculus

SUBMITTER: Tomoaki Ando

PROVIDER: E-GEOD-53132 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Der f/SEB-induced skin inflammation

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.

2013-12-10 | GSE53132 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of Stat3f/f K5cre Skin Keratinocytes Transcriptomes

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 NFB 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

Untargeted lipidomics studies in the course of dermatitis onset and progression

Project description:We applied untargeted lipidomic analysis to the atopic dermatitis-like dermatitis model (Spade mice) to capture the comprehensive lipidome profile in the course of dermatitis onset and progression. Spade mice harbor a single amino acid mutation in Jak1 that causes hyperactivation, leading to Th2 dermatitis. Progressive dermatitis develops as desquamation and redness of the ears at approximately 8 weeks of age. At 10 weeks of age, serum IgE and IgG1 levels are increased, and Th2 cytokines, such as IL-4, IL-5, and IL-13, produced by CD4+ cells are upregulated, followed by elevated serum histamine levels at 12 weeks of age. Skin lesions manifest as epidermal hyperplasia at 8 weeks of age, while there are few morphological changes at 4 weeks of age. TEWL, the readout for barrier function, is significantly elevated in Spade mice at 4 weeks of age, suggesting that barrier defects had occurred before disease onset. WT and Spade skin tissues in P0, 4, 8, and 10 weeks of age were applied to untargeted lipidomics. Over 700 skin lipids including glycerophospholipids, ceramides, neutral lipids, and fatty acids were successfully annotated, and many of them were found to be significantly changed after dermatitis onset as determined by pruritus and erythema. Among them, the levels of Cer[NdS] containing very long-chain (C22 or more) fatty acids were significantly downregulated before AD onset.

2022-05-25 | ST002195 | MetabolomicsWorkbench

Upper airway gene expression is an effective surrogate biomarker for Th2-driven inflammation in the lower airway

Project description:Molecular profiling studies in asthma cohorts have identified a Th2-driven asthma subtype, characterized by elevated lower airway expression of POSTN, CLCA1 and SERPINB2. To assess upper airway gene expression as a potential biomarker for lower airway Th2 inflammation, we assayed upper airway (nasal) and lower airway (bronchial) epithelial gene expression, serum total IgE, blood eosinophils and serum periostin in a cohort of 54 allergic asthmatics and 30 matched healthy controls. 23 of 51 asthmatics in our cohort were classified as âTh2 highâ based on lower airway Th2 gene signature expression. Consistent with this classification, âTh2 highâ subjects displayed elevated total IgE and blood eosinophil levels relative to âTh2 lowâ subjects. Upper airway Th2 signature expression was significantly correlated with lower airway Th2 signature expression (r=0.44), with similar strength of association as serum total IgE and blood eosinophils, known biomarkers of Th2 inflammation. In an unbiased genome-wide scan, we identified 8 upper airway genes more strongly correlated with lower airway Th2 gene signature expression (r=0.58), including Eotaxin-3 (CCL26), Galectin-10 (CLC) and Cathepsin-C (CTSC). Asthmatics classified as âTh2 highâ using this 8-gene signature show similar serum total IgE and blood eosinophil levels as âTh2 highâ asthmatics classified using lower airway Th2 gene signature expression. We have identified an 8-gene upper airway signature correlated with lower airway Th2 inflammation, which may be used as a diagnostic biomarker for Th2-driven asthma. Upper airway (nasal) and lower airway (bronchial) epithelial brushings obtained from a cohort of 54 allergic asthmatics and 30 matched healthy controls were profiled by gene expression by microarray. Subjects were assayed for gene expression, serum total IgE, blood eosinophils and serum periostin.

2015-10-23 | E-GEOD-41861 | biostudies-arrayexpress

T-bet and STAT6 Coordinately Suppress the Development of IL-9-mediated Atopic Dermatitis-like Skin Inflammation in Mice

Project description:T-bet and STAT6 are critical factors for helper T cell differentiation in humans and mice. Additionally, polymorphisms in TBX21 (T-bet) and STAT6 are associated with the susceptibility of allergic diseases. However, precise mechanisms of the reciprocal regulation between T-bet and STAT6 in allergy remain unclear. To determine the reciprocal regulation in vivo, we investigated the phenotype of T-bet/STAT6 double-deficient (T-bet-/- STAT6-/-) mice. Unexpectedly, T-bet-/- STAT6-/- mice but not T-bet-/- mice or STAT6-/- mice spontaneously developed severe dermatitis. Not only eosinophils and mast cells but also CD4+ T cells infiltrated into the skin of T-bet-/- STAT6-/- mice. Adoptive transfer of CD4+ T cells of T-bet-/- STAT6-/- mice into SCID mice induced the accumulation of eosinophils and mast cells in the skin, while depletion of CD4+ T cells ameliorated the dermatitis in T-bet-/- STAT6-/- mice. Comprehensive transcriptome analyses revealed that IL-9 expression was enhanced in T-bet-/- STAT6-/- CD4+ T cells. Indeed, IL-9 neutralization ameliorated the dermatitis in T-bet-/- STAT6-/- mice. Importantly, T-bet-/- STAT6-/- CD4+ T cells expressed functional TSLP receptor and produced large amounts of IL-9 upon TSLP stimulation. These results indicate that T-bet and STAT6 suppress atopic dermatitis-like skin inflammation, possibly by inhibiting TSLP-dependent IL-9 production in CD4+ T cells.

2020-08-15 | GSE156288 | GEO

Immunological Proteome Resource (ImmPRes): Part two

Project description:Second dataset release from the Immunological Proteome Resource (ImmPRes). This dataset contains both lymphoid and myeloid populations. The whole list is as follows: Bone marrow derived eosinophils, bone marrow derived mast cells, bone marrow derived macrophages, NK cells, TH2 cells, TH17 cells, Cytotoxic T cells cultured in IL15 and Naive CD8+ T cells extractred from the lymph nodes of C57BL/6J mice.

2020-07-02 | PXD020091 | Pride

Next Generation Sequencing Facilitates Quantitative Analysis of mRNA expression of STAT3 deficiency skin

Project description:Dominant-negative mutations of signal transducer and activator of transcription 3 (STAT3) signaling which controls epithelial proliferation in various tissues, leads to atopic dermatitis (AD) in hyper IgE syndrome (HIES). We found that the STAT3 signaling in keratinocytes is required to maintain skin homeostasis through this transcriptome analysis.

2021-10-15 | GSE185585 | GEO

Eftimie2010 - immunity to melanoma

Project description:The paper describes a model of immunity to melanoma. Created by COPASI 4.25 (Build 207) This model is described in the article: Modeling anti-tumor Th1 and Th2 immunity in the rejection of melanoma Raluca Eftimie, Jonathan L. Bramson, David J.D. Earn Journal of Theoretical Biology 265 (2010) 467–480 Abstract: Recent experiments indicate that CD4+ Th2 cells can reject skin tumors in mice, while CD4+ Th1 cells cannot (Mattes et al., 2003; Zhang et al., 2009). These results are surprising because CD4+ Th1 cells are typically considered to be capable of tumor rejection. We used mathematical models to investigate this unexpected outcome. We found that neither CD4+ Th1 nor CD4+ Th2 cells could eliminate the cancer cells when acting alone, but that tumor elimination could be induced by recruitment of eosinophils by the Th2 cells. These recruited eosinophils had unexpected indirect effects on the decay rate of type 2 cytokines and the rate at which Th2 cells are inactivated through interactions with cancer cells. Strikingly, the presence of eosinophils impacted tumor growth more significantly than the release of tumor-suppressing cytokines such as IFN-g and TNF-a. Our simulations suggest that novel strategies to enhance eosinophil recruitment into skin tumors may improve cancer immunotherapies. To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models . To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information.

2019-07-30 | BIOMD0000000768 | BioModels

Upper airway gene expression is an effective surrogate biomarker for Th2-driven inflammation in the lower airway

Project description:Molecular profiling studies in asthma cohorts have identified a Th2-driven asthma subtype, characterized by elevated lower airway expression of POSTN, CLCA1 and SERPINB2. To assess upper airway gene expression as a potential biomarker for lower airway Th2 inflammation, we assayed upper airway (nasal) and lower airway (bronchial) epithelial gene expression, serum total IgE, blood eosinophils and serum periostin in a cohort of 54 allergic asthmatics and 30 matched healthy controls. 23 of 51 asthmatics in our cohort were classified as ‘Th2 high’ based on lower airway Th2 gene signature expression. Consistent with this classification, ‘Th2 high’ subjects displayed elevated total IgE and blood eosinophil levels relative to ‘Th2 low’ subjects. Upper airway Th2 signature expression was significantly correlated with lower airway Th2 signature expression (r=0.44), with similar strength of association as serum total IgE and blood eosinophils, known biomarkers of Th2 inflammation. In an unbiased genome-wide scan, we identified 8 upper airway genes more strongly correlated with lower airway Th2 gene signature expression (r=0.58), including Eotaxin-3 (CCL26), Galectin-10 (CLC) and Cathepsin-C (CTSC). Asthmatics classified as ‘Th2 high’ using this 8-gene signature show similar serum total IgE and blood eosinophil levels as ‘Th2 high’ asthmatics classified using lower airway Th2 gene signature expression. We have identified an 8-gene upper airway signature correlated with lower airway Th2 inflammation, which may be used as a diagnostic biomarker for Th2-driven asthma.

2015-10-23 | GSE41861 | GEO

Proinflammatory role of histamine-releasing factor in asthma and allergy

Project description:Immunoglobulin (Ig) E-mediated activation of mast cells and basophils underlies allergic diseases such as asthma. Histamine-releasing factor (HRF), also known as translationally controlled tumor protein (TCTP) and fortilin, is a highly conserved protein with both intracellular and extracellular functions. Secreted HRF can stimulate histamine release and IL-4 and IL-13 production from IgE-sensitized basophils and mast cells. HRF is found in nasal, skin blister and bronchoalveolar lavage (BAL) fluids during late-phase allergic reactions (LPRs), which implicates HRF in the LPR and chronic allergic inflammation. Here we identify a subset of IgE and IgG antibodies as HRF-interacting molecules. HRF can exist as a dimer and bind to immunoglobulins (Igs) via interactions of its N-terminal and internal regions with the Fab region of Igs. Therefore, HRF together with HRF-reactive IgE can activate mast cells in vitro. The Ig-interacting HRF peptides that block HRF-Ig interactions can inhibit IgE+HRF-induced mast cell activation and in vivo cutaneous anaphylaxis and airway inflammation. Intranasally administered HRF can recruit inflammatory immune cells to the lung in naïve mice in a mast cell- and Fc receptor-dependent manner. These results strongly suggest the proinflammatory role of HRF in asthma and skin immediate hypersensitivity. A total of 6 samples were analyzed; wild type C57BL/6, FcRg KO and FceRIa KO mice were challenged with PBS (control) or mouse histamien-releasing factor

2011-12-04 | E-GEOD-34133 | biostudies-arrayexpress

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