Identification of Pre-Disease State in NC/Nga Mice with Atopic dermatitis-like Symptoms using Dynamical Network Biomarkers
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PROVIDER: PRJNA1253655 | ENA |
REPOSITORIES: ENA
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Project description:Atopic dermatitis (AD) is a common skin disease worldwide characterized by itchy eczema that undergoes cycles of exacerbation and remission. While several biomarkers reflect AD severity, reliable markers for predicting disease onset and recurrence remain unclear. The dynamical network biomarker (DNB) theory, which detects pre-disease states, or pre-symptomatic states by analyzing characteristic network fluctuations just before phase transitions from healthy states to disease states. To investigate the applicability of DNB theory to AD, we conducted blood transcriptome analysis in NC/Nga mice before and after the onset of AD-like dermatitis. We identified 356 DNB genes whose temporal fluctuations enabled the detection of the pre-disease state preceding AD-like dermatitis onset. These genes were significantly enriched in pathways related to endoplasmic reticulum stress and apoptosis; fluctuations in these pathways may be associated with the onset of AD. Our study indicates that the DNB theory may be applicable to AD and that identifying a pre-disease state may enable early intervention and disease prevention. Collectively, this approach could provide valuable insights into maintaining long-term remission and improving AD management strategies.
2025-09-09 | GSE295168 | GEO
Project description:Gene expression data from atopic dermatitis induced NC/Nga mouse model skin
| PRJNA512476 | ENA
Project description:We identified zinc-alpha-2-glycoprotein (ZAG), a 41-kDa adipokine that regulates body weight, lipid, and mobilization, as a novel biomarker for AD. ZAG levels were consistently decreased in sera, T cells, and skin in human AD patients compared with healthy controls. We used microarrays to obtain the change of signaling molecules by topical treatment of recombinant ZAG using atopic dermatitis induced mouse model.
2019-01-03 | GSE124550 | GEO
Project description:Interleukin-7 (IL-7) plays a vital role in the homeostasis of CD4+ and CD8+ T cells. Although IL-7 has been implicated in T helper (Th)1- and Th17-mediated autoinflammatory diseases, its role in Th2-type allergic disorders, such as atopic dermatitis (AD), remains unclear. Thus, to elucidate the effects of IL-7 deficiency on AD development, we generated IL-7-deficient AD-prone mice by backcrossing IL-7 knockout (KO) B6 mice onto the NC/Nga (NC) mouse strain, a model for human AD. As expected, IL-7 KO NC mice displayed defective development of conventional CD4+ and CD8+ T cells compared with wild type (WT) NC mice. However, IL-7 KO NC mice presented with enhanced AD clinical scores, IgE hyperproduction, and increased epidermal thickness compared with WT NC mice. Moreover, IL-7 deficiency decreased Th1, Th17, and IFN-γ-producing CD8+ T cells but increased Th2 cells in the spleen of NC mice, indicating that a reduced Th1/Th2 ratio correlates with severity of AD pathogenesis. Furthermore, significantly more basophils and mast cells infiltrated the skin lesions of IL-7 KO NC mice. Taken together, our findings suggest that IL-7 could be a useful therapeutic target for treating Th2-mediated skin inflammations, such as AD.
| S-EPMC10298193 | biostudies-literature
Project description:Various factors have been reported to influence lipid metabolism and cause metabolic syndrome. However, the influence of allergy on the liver that plays important role of lipid metabolism has not been clarified. The aim of this study was to examine the influence of allergy on lipid metabolism of liver. A model of atopic dermatitis was developed in the NC/Nga mouse using picryl chloride to induce allergy. Lipid metabolism parameters were measured and the mechanism of changes in these parameters was examined using DNA microarray analysis and quantitative reverse transcriptase PCR. Triacylglycerol accumulation was promoted in the liver in the mouse atopic dermatitis model despite reductions in food intake, body weight gain, and serum glucose. As this mechanism, it was thought that atopic dermatitis caused the suppression of fatty acid β-oxidation. These results suggest that atopic dermatitis causes lipid accumulation in the liver.
| S-EPMC3303478 | biostudies-literature
Project description:BackgroundIn the current study, we evaluated whether atopic dermatitis (AD) affects the entire body rather than being limited to skin barrier damage and inflammation. We hypothesized that medium-term exposure of distant organs to systemic inflammatory cytokines in sub-chronic inflammatory skin diseases has detrimental effects on distant tissues.ResultsOur findings demonstrated the dysregulation of genes and pathways associated with inflammation and the skin barrier, as well as genes and pathways involved in muscle development that respond to chemicals or stress in muscle tissues, all of which were reversed by hydrocortisone (Hc) administration. The expression of Ces1d showed significant differences during disease onset and after treatment in both skin and skeletal muscle, suggesting that Ces1d is likely responsible for the alleviation of subchronic AD.ConclusionsUsing NC/Nga mice with AD-like symptoms, we compared the transcriptomes of the skeletal muscle (a tissue that is relatively distant from the skin) with those of the skin (the lesion induction site) before and after disease induction, after which Hc was administered. Although further study is needed to better understand the effects of Ces1d on AD, skeletal muscle was associated with AD pathogenesis, and AD-like symptoms appeared to affect the body in a systemic manner. Given the importance of evidence-based medicine and the development of precision medicine, our findings provide insights into the mechanisms of AD onset and progression.
| S-EPMC11544999 | biostudies-literature
Project description:BackgroundAtopic diseases are more prevalent in industrialized countries than in developing countries. In addition, significant differences in the prevalence of allergic diseases are observed between rural and urban areas within the same country. This difference in prevalence has been attributed to what is called the 'hygiene hypothesis'. Although parasitic infections are known to protect against allergic reactions, the mechanism is still unknown. The aim of this study was to investigate whether or not malarial infections can inhibit atopic dermatitis (AD)-like skin lesions in a mouse model of AD.MethodsWe used NC/Nga mice which are a model for AD. The NC/Nga mice were intraperitoneally infected with 1 × 10(5) Plasmoduim berghei (Pb) XAT-infected erythrocytes.ResultsMalarial infections ameliorated AD-like skin lesions in the NC/Nga mice. This improvement was blocked by the administration of anti-asialo GM1 antibodies, which are anti-natural killer (NK) cells. Additionally, adoptive transfer of NK cells markedly improved AD-like skin lesions in conventional NC/Nga mice; these suggest that the novel protective mechanism associated with malaria parasitic infections is at least, in part, dependent on NK cells.ConclusionsWe have experimentally demonstrated for the first time that malarial infections ameliorated AD-like skin lesions in a mouse model of AD. Our study could explain in part the mechanism of the 'hygiene hypothesis', which states that parasitic infections can inhibit the development of allergic diseases.
| S-EPMC4329412 | biostudies-literature
Project description:Forsythia suspensa (F. suspensa) is a traditional medicine for treatment of inflammation. In this study, we evaluated the therapeutic effects of an ethanol extract from F. suspensa fruits on atopic dermatitis both in vivo and in vitro. We investigated the inhibitory effects of F. suspensa extract on the development of atopic dermatitis-like skin lesions in an NC/Nga mouse model exposed to Dermatophagoides farinae crude extract. Topical application of F. suspensa extract to the mice attenuated the atopic dermatitis symptoms, including increased dermatitis severity score, ear thickness, infiltration of inflammatory cells in the skin lesions, serum levels of IgE, TNF-α, and histamine, and expression of chemokines, cytokines, and adhesion molecules in ear tissue. In addition, F. suspensa extract inhibited the production of chemokines in TNF-α/IFN-γ-activated human keratinocytes. High-performance liquid chromatography analysis of FSE revealed the presence of four chemical constituents (forsythiaside, phillyrin, pinoresinol, and phylligenin). These compounds inhibited the production of chemokines in TNF-α/IFN-γ-activated human keratinocytes. These results suggest that the F. suspensa might be a useful candidate for treating allergic skin inflammatory disorders.
| S-EPMC5147941 | biostudies-literature
Project description:In this study we applied genomic profiling to evaluate the transcriptomic differences between murine models ot atopic dermatitis. We evaluated the expression data of five models and their respective controls, and one previously published murine dataset (GSE50400). The included models were groupe 1 (Lesional: Flaky tail and FLG mutant; Control: C57BL/6NCrSlc), Group 2 (Lesional: NC/Nga(+mite); Control: NC/Nga(-mite)), Group 3 (Lesional: OVA-ODT 24h; Control: C57BL/6NCrSlc), and Group 4 (Lesional: OXA 2h; Control: BALB/c,Acetone).
2017-01-02 | GSE81119 | GEO