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Temporal Gene Expression Patterns in the skin of D6 null and wild type mice after inflammation with the chemical irritant TPA

ABSTRACT: The chemokine decoy receptor D6 internalises and degrades inflammatory CC chemokines enabling resolution of inflammation. In D6 deficient mice (D6 KO), otherwise innocuous cutaneous inflammatory stimuli induce a grossly exaggerated inflammatory response that bears many similarities to human psoriasis. In the present study we have used transcriptomic approaches to define the molecular make up of this response. The result of such analysis highlights potential roles for a number of cytokines iniating and maintaining psoriasis like pathology. Most compellingly, we provide data indicating a key role for the type I interferon pathway in the emergence of this pathology

ORGANISM(S): Mus musculus

PROVIDER: GSE46889 | GEO | 2013/05/28

SECONDARY ACCESSION(S): PRJNA205534

REPOSITORIES: GEO

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Temporal Gene Expression Patterns in the skin of D6 null and wild type mice after inflammation with the chemical irritant TPA

Project description:The chemokine decoy receptor D6 internalises and degrades inflammatory CC chemokines enabling resolution of inflammation. In D6 deficient mice (D6 KO), otherwise innocuous cutaneous inflammatory stimuli induce a grossly exaggerated inflammatory response that bears many similarities to human psoriasis. In the present study we have used transcriptomic approaches to define the molecular make up of this response. The result of such analysis highlights potential roles for a number of cytokines iniating and maintaining psoriasis like pathology. Most compellingly, we provide data indicating a key role for the type I interferon pathway in the emergence of this pathology Backskin of D6 null mice was painted with three successive applications of 50uM TPA (in acetone), 24 hours apart. Control (labelled as day 0 or untreated) were treated with acetone only. After the three successive applications of TPA, pathology was left to develop for 1, 2, 4 or 6 days and backskin was taken for microarray analysis at each of these time points. To identify differentially expressed genes, comparisons were made between D6 KO and WT mice at each time point (D6 KO vs WT mice at day 0, day 1, day 2, day 4 or day 6). Significantly differentially expressed genes (p<0.05 according to an unpaired t-test) and up or down regulated more than 3 fold were identified ay each time point and selected for further analysis.

2013-05-28 | E-GEOD-46889 | biostudies-arrayexpress

Alteration of renal gene expression affected by atypical chemokine receptor D6 knockout in diabetic OVE26 (OVE) mice

2013-10-10 | GSE51205 | GEO

Alteration of renal gene expression affected by atypical chemokine receptor D6 knockout in diabetic OVE26 (OVE) mice

Project description:The D6 receptor can bind and internalize inflammatory chemokines without activating intracellular pathways. D6 can reduce tissue inflammation, presumably by scavenging inflammatory chemokines. In diabetic kidney there is extensive inflammation but the possible role of the D6 receptor has never been tested. In this study, we included the renal gene expression dataset generated from whole kidney RNA extraction in diabetic mice with or without D6 gene knockout, their controls are age and sex matched D6 deficient or wild type mice on FVB background. These data are used to analyze the effects of D6 deletion on progression of diabetic nephropathy. D6 knockout mice were crossing with FVB stain to produce D6 knockout mice in FVB background (D6). Then D6 was crossed with diabetic mice (OVE) to produce D6 defficient diabetic mice (OVE-D6). These mice were followed up for albuminuria from 2 month old, and sacrificied at 6 months for gene expression and renal morphology analysis. 12 kidney samples (3 per group) were used in this gene array study.

2013-10-10 | E-GEOD-51205 | biostudies-arrayexpress

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Devosia sp. D6-9

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Environmental factors transmitted by aryl hydrocarbon receptor influence severity of psoriatic skin inflammation [Affymetrix]

Project description:Environmental stimuli are known to contribute to psoriasis pathogenesis and that of other autoimmune diseases, but the mechanism is unknown. Here we show that the aryl hydrocarbon receptor (AhR), a transcription factor that senses environmental stimuli, modulates pathology in psoriasis. AhR-activating ligands reduced inflammation in the lesional skin of psoriasis patients, whereas AhR antagonists upregulated inflammation. Similarly, AhR signaling via the endogenous FICZ ligand reduced the inflammatory response in the imiquimod-induced model of psoriasis and AhR deficient mice exhibited a substantial exacerbation of the disease, compared to AhR sufficient controls. Non-haematopoietic cells, in particular keratinocytes, were responsible for this hyper-inflammatory response, which involved increased reactivity to IL-1beta and upregulation of AP-1 family members of transcription factors. Thus, our data suggest a critical role for AhR in the regulation of inflammatory responses and open the possibility for novel therapeutic strategies in chronic inflammatory disorders. Total RNA obtained from skin explants taken from AhR heterozygous or knock-out mice treated pericutaneously with imiquimod for 0 and 2d.

2014-06-11 | E-GEOD-47607 | biostudies-arrayexpress

Environmental factors transmitted by aryl hydrocarbon receptor influence severity of psoriatic skin inflammation [RNA-Seq]

Project description:Environmental stimuli are known to contribute to psoriasis pathogenesis and that of other autoimmune diseases, but the mechanism is unknown. Here we show that the aryl hydrocarbon receptor (AhR), a transcription factor that senses environmental stimuli, modulates pathology in psoriasis. AhR-activating ligands reduced inflammation in the lesional skin of psoriasis patients, whereas AhR antagonists upregulated inflammation. Similarly, AhR signaling via the endogenous FICZ ligand reduced the inflammatory response in the imiquimod-induced model of psoriasis and AhR deficient mice exhibited a substantial exacerbation of the disease, compared to AhR sufficient controls. Non-haematopoietic cells, in particular keratinocytes, were responsible for this hyper-inflammatory response, which involved increased reactivity to IL-1beta and upregulation of AP-1 family members of transcription factors. Thus, our data suggest a critical role for AhR in the regulation of inflammatory responses and open the possibility for novel therapeutic strategies in chronic inflammatory disorders. Total RNA obtained from skin explants taken from psoriatic patients or healthy donors cultured in the presence of AhR agonist or antagonist

2014-06-11 | E-GEOD-47944 | biostudies-arrayexpress

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