Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA341396 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR4106150.fastq.gz | Fastqsanger.gz | |||
| SRR4106160.fastq.gz | Fastqsanger.gz | |||
| SRR4106170.fastq.gz | Fastqsanger.gz | |||
| SRR4106180.fastq.gz | Fastqsanger.gz | |||
| SRR4106190.fastq.gz | Fastqsanger.gz |
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Project description:The polyphenol resveratrol has anti-inflammatory effects in various cells, tissues, animals and human settings of low-grade inflammation. Psoriasis is a disease of both localized and systemic low-grade inflammation. The Sirtuin1 enzyme thought to mediate the effects of resveratrol is present in skin and resveratrol is known to downregulate NF-κB; a major contributor in the development of psoriasis. Consequently we investigated whether resveratrol has an effect on an Imiquimod induced psoriasis-like skin inflammation in mice and sought to identify candidate genes, pathways and interleukins mediating the observed effects. The study consisted of three treatment groups: A control group, an Imiquimod group and an Imiquimod+resveratrol group. Psoriasis severity was assessed using elements of the Psoriasis Area Severity Index, actual skin thickness measurements, and histological examination. We performed an RNA microarray from lesional skin and afterwards Ingenuity pathway analysis to identify affected signalling pathways. Our microarray was compared to a previously deposited microarray to determine if gene changes were psoriasis-like, and to a human microarray to determine if findings could be relevant in a human setting. Imiquimod treatment induced a psoriasis-like skin inflammation. Resveratrol significantly diminished the severity of the psoriasis-like skin inflammation. The RNA microarray revealed a psoriasis-like gene expression-profile in the Imiquimod treated group, and highlighted several resveratrol dependent changes in relevant genes, such as increased expression of genes associated with retinoic acid stimulation and reduced expression of genes involved in IL-17 dependent pathways (e.g.IL-17A, IL-17F,IL-23p19 ). Quantitative PCR confirmed a resveratrol dependent decrease in mRNA levels of IL-17A and IL-19; both central in developing psoriasis. In conclusion, resveratrol ameliorates psoriasis, and changes in expression of retinoic acid stimulated genes, IL-17 signalling pathways, IL-17A and IL-19 mRNA levels in a beneficial manner suggests it might have a role in the treatment of psoriasis and should be explored further in a human setting.
2015-11-17 | GSE63684 | GEO
Project description:Increased intestinal permeability can exacerbate psoriasis, a systemic inflammatory disease with complex pathogenesis. Using a mouse model of psoriasis elicited by the TLR7 ligand imiquimod, we found that psoriatic dermatitis was accompanied by small-intestinal inflammatory changes associated with eosinophil degranulation which led to impaired intestinal barrier integrity. Inflammatory responses in the skin and small intestine were accelerated in mice that are prone to eosinophil degranulation. Caco-2 human intestinal epithelial cells treated with media containing eosinophil granule proteins exhibited signs of inflammation and damage. Imiquimod-induced skin and intestinal inflammatory changes were attenuated in eosinophil-deficient mice, and this attenuation was counteracted by eosinophil transfer. Imiquimod levels and eosinophil distribution were positively correlated in the intestine. TLR7-deficient mice did not show intestinal eosinophil degranulation and exhibited attenuated skin and small-intestinal inflammation following imiquimod application. These results suggest a TLR7-dependent bidirectional skin-to-gut communication in psoriatic inflammation, and that intestinal inflammatory changes can accelerate psoriasis.
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Project description:Resveratrol ameliorates Imiquimod-induced psoriasis-like skin inflammation in mice
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Project description:Background: Imiquimod (IMQ) produces a cutaneous phenotype in mice frequently studied as an acute model of human psoriasis. Whether this phenotype depends on strain or sex has never been systematically investigated on a large scale. Such effects, however, could lead to conflicts among studies, while further impacting study outcomes and efforts to translate research findings. Methods: RNA-seq was used to evaluate the psoriasiform phenotype elicited by IMQ in both sexes of 7 mouse strains (C57BL/6J, BALB/cJ, CD1, DBA/1J, FVB/NJ, 129X1/SvJ and MOLF/EiJ). Results: In most strains, IMQ altered gene expression in a manner consistent with human psoriasis, partly due to innate immune activation and decreased homeostatic gene expression. The IMQ response of MOLF males was aberrant, however, with decreased expression of differentiation-associated genes (elevated in other strains). Key aspects of the IMQ response differed between the two most commonly studied strains (BALB/c and C57BL/6). Compared with BALB/c, the C57BL/6 phenotype showed increased expression of genes associated with DNA replication, IL-17A activation and CD8+ T cells, but decreased expression of genes associated with interferon signaling and CD4+ T cells. Surprisingly, although IMQ-induced expression shifts mirrored psoriasis, correspondence was similar or better for other human skin diseases (e.g., eschars, acne, atopic dermatitis). For BALB/c, MOLF, and 129X1 strains, genes altered by IMQ corresponded better to those altered in human skin infections or wounds compared with those altered in psoriasis lesions. Conclusions: These findings demonstrate strain-dependent aspects of IMQ dermatitis that warrant consideration in planning and interpreting experimental studies. We have further shown that IMQ does not uniquely model psoriasis but in fact triggers a core set of pathways active in diverse skin diseases. These observations challenge the view of IMQ dermatitis as a mouse phenotype uniquely appropriate for studying psoriasis as opposed to other human skin conditions.
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Project description:The imiquimod model is used to induce the skin production of IL-22 and to characterize the cells that produce IL-22 in the skin after inflammatory stimulus. This experiment is performed on skin of C57Bl/6 mice treated with imiquimod to induce psoriasis-like lesions. After 5 days of imiquimod treatment, we analysed the heamatopoietic cells that infiltrate the skin and we compared the gene signature of three T cell populations: CD4+ T cells, CD4-CD8-(DN) T cells and gd T cells
2016-08-09 | E-MTAB-4453 | biostudies-arrayexpress
Project description:RNA-seq of imiquimod-Induced psoriasis-like mice using Sicao Oil
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Project description:We analyzed epidermal samples from keratinocyte-specific knockout Mettl3 (K14CreERT2;Mettl3fl/fl) mice and their controls (Mettl3fl/fl) in imiquimod-induced psoriasis-like skin lesions. Briefly, we established an imiquimod-induced psoriasis model in K14CreERT2;Mettl3fl/fl mice and their controls after tamoxifen injection, and epidermal samples were separated and collected from the skin lesions of the mice after 3 or 6 days of modeling (n=3 per group). The aim of this study was to investigate the mechanism by which Mettl3-mediated epidermal m6A methylation affects skin inflammation.
2024-08-20 | GSE268745 | GEO
Project description:Psoriasis is one of the most common dermatological disorders, characterized by increased epidermal hyperplasia and immune cell infiltration. Psychological stress has been reported to contribute to the severity, aggravation, and relapse of psoriasis. We developed a chronic restrain stress (CRS)-imiquimod (IMQ)-induced psoriasis-like mouse model and performed a comprehensive comparative transcriptomic and metabolic analysis with control mice, CRS-treated mice, and IMQ-treated mice to investigate how psychological stress affects psoriasis. We found that CRS-IMQ-induced psoriasis-like mice showed significant exacerbation of psoriasis-like skin inflammation compared with mice treated with IMQ only. Mice of the CRS+IMQ group showed increased expression of keratinocyte proliferation and differentiation genes, differential regulation of cytokines, and promotion of the linoleic acid metabolism. Our study provides new insights into the effects of psychological stress on psoriasis pathogenesis and the mechanisms involved, which provides clues for development of therapeutics or biomarkers.
2022-12-31 | GSE212126 | GEO
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.
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