Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of mouse skin treated with ovalbumin to induce atopic dermatitus and then treated with a test drug or ramatroban or dexamethasone

ABSTRACT: A highly specific and potent small molecule antagonist of CRTH2 (chemoattractant receptor) was used to investigate the role of this Prostaglandin D2 (PGD2) receptor in chronic models of cutaneous inflammation and the underlying immune response. These RNA samples are from mice that were in a chronic (50 day) model of atopic dermatitis. Each mouse had a section of back skin patched with a gauze, and the RNA was from the patched area of skin; the control mice had the gauze soaked in PBS, whereas all the other test mice had the gauze soaked in ovalbumin dissolved in PBS. The ovalbumin acts as an allergen and induces the experimental atopic dermatitis. The six groups of mice that received the OVA patch were treated in different ways:some received just the drug vehicle during the OVA patching, others received the test drug (compound A) at 3 different concentrations: 10 mg/kg 1 mg/kg and 0.1 mg/kg. Two other cohorts received positive control drugs: ramatroban and dexamethasone .Each different sample represents a different animal.

ORGANISM(S): Mus musculus

SUBMITTER: Narimene Lekmine

PROVIDER: E-TABM-505 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Murine Pulmonary Responses to Ambient Baltimore Particulate Matter: Genomic Analysis and Contribution to Airway Hyperresponsiveness; Asthma is a complex disease characterized by airway hyperresponsiveness (AHR) and chronic airway inflammation. Environmental factors such as ambient particulate matter (PM), a major air pollutant, has been demonstrated in epidemiological studies to contribute to asthma exacerbation and increased asthma prevalence. OBJECTIVE: We investigated the genomic and pathophysiological effects of Baltimore PM (median diameter 1.78 Âµm) in a murine model of asthma to identify potential biomarkers. METHODS: A/J mice with ovalbumin (OVA) âinduced AHR were exposed to PM (20 mg/kg, intratracheal), and both AHR and bronchoalveolar lavage (BAL) were assayed on days 1, 4, and 7 post exposure. Lung gene expression profiling (Affymetrix Mouse430_ 2.0) by PM (20 mg/kg, intratracheal) were assayed on OVA- and / or PM--challenged mice. RESULTS: Significant increases of airway responsiveness in OVA-treated mice were observed, indicating an asthmatic phenotype. Ambient PM exposure induced significant changes in AHR in both naive mice and OVA-induced asthmatic mice. In both naive and OVA challenged asthmatic mice, PM induced eosinophil and neutrophil infiltration into airways, elevated BAL protein content, and stimulated secretion of TH1 cytokines (IFN-g, IL-6, and TNF-a) and TH2 cytokines (IL-4, IL-5, and eotaxin) into BAL. Consistent with these results, PM induced expression of genes of innate immune response, chemotaxis and complementary system. CONCLUSION: These studies, consistent with epidemiological data, indicate that PM increases AHR and lung inflammation in naÃ¯ve mice and exacerbates the asthma phenotype of increased AHR and gene expression pattern changes correlated with acute lung inflammation and airway damage. We used microarrays to detail the global programme of gene expression induced by rhPBEF treatment and VALI. Experiment Overall Design: animals were treated by PBS, Oval albumin, PM, or both OVA/PM

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Transcription profiling of mouse skin treated with ovalbumin to induce atopic dermatitus and then treated with a test drug or ramatroban or dexamethasone

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