Similar Datasets
Project description:Skin microbiota of an oxazolone-induced contact hypersensitivity mouse model
| PRJNA874845 | ENA
Project description:Psoriasis-like skin inflammation was indused by 5 daily topical applications of imiquimod (IMQ), a TLR7/8 agonist, or vehicle, in mice fed a high fat diet (HFD) or control chow diet (CD). Skin samples were collected at day 6.
2019-06-30 | GSE68750 | GEO
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:Single-Cell RNA-seq immune profile of normal and inflammed mouse skin
| PRJNA627418 | ENA
Project description:TREX2 is a keratinocyte specific 3â-deoxyribonuclease that participates in the maintenance of skin homeostasis upon damage. This transcriptome analysis identified multiple genes and pathways deregulated by TREX2 loss in the IMQ-induced psoriasis-like model in mouse skin. mRNA sequencing of 5 biological replicates of skin from wild-type mice treated with Imiquimod and 6 of Trex2 knockout mice treated with Imiquimod
2016-09-07 | E-GEOD-74528 | biostudies-arrayexpress
Project description:Development of a suitable mouse model would facilitate the investigation of pathomechanisms underlying human psoriasis and would also assist in development of therapeutic treatments. However, while many psoriasis mouse models have been proposed, no single model recapitulates all features of the human disease, and standardized validation criteria for psoriasis mouse models have not been widely applied. In this study, whole-genome transcriptional profiling is used to compare gene expression patterns manifested by human psoriatic skin lesions with those that occur in five psoriasis mouse models (K5-Tie2, imiquimod, K14-AREG, K5-Stat3C and K5-TGFbeta1). While the cutaneous gene expression profiles associated with each mouse phenotype exhibited statistically significant similarity to the expression profile of psoriasis in humans, each model displayed distinctive sets of similarities and differences in comparison to human psoriasis. For all five models, correspondence to the human disease was strong with respect to genes involved in epidermal development and keratinization. Immune and inflammation-associated gene expression, in contrast, was more variable between models as compared to the human disease. These findings support the value of all five models as research tools, each with identifiable areas of convergence to and divergence from the human disease. Additionally, the approach used in this paper provides an objective and quantitative method for evaluation of proposed mouse models of psoriasis, which can be strategically applied in future studies to score strengths of mouse phenotypes relative to specific aspects of human psoriasis. Global transcriptional profiling was utilized to evaluate the similarity between human psoriasis and the psoriasis-like phenotypes that develop in five mouse models (K5-Tie2, IMQ, K14-AREG, K5-Stat3C, K5-TGFbeta1) Expression patterns associated with mouse phenotypes were evaluated by comparing lesional skin from transgenic or IMQ-treated mice (n = 2-3) with normal skin obtained from control mice (n = 2-3).
2011-03-03 | E-GEOD-27628 | biostudies-arrayexpress
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.
2024-04-30 | GSE237610 | GEO
Project description:Epidermal or dermal cell suspensions from imiquimod-induced C57BL/6 mice were subject to single-cell RNA-seq.
2022-06-14 | GSE205790 | GEO
Project description:Determine how regulatory T-cells restrain the cellular/transcriptional response to Imiquimod treatment in the skin (ears).
2018-06-24 | E-MTAB-6873 | biostudies-arrayexpress
Project description:Development of a suitable mouse model would facilitate the investigation of pathomechanisms underlying human psoriasis and would also assist in development of therapeutic treatments. However, while many psoriasis mouse models have been proposed, no single model recapitulates all features of the human disease, and standardized validation criteria for psoriasis mouse models have not been widely applied. In this study, whole-genome transcriptional profiling is used to compare gene expression patterns manifested by human psoriatic skin lesions with those that occur in five psoriasis mouse models (K5-Tie2, imiquimod, K14-AREG, K5-Stat3C and K5-TGFbeta1). While the cutaneous gene expression profiles associated with each mouse phenotype exhibited statistically significant similarity to the expression profile of psoriasis in humans, each model displayed distinctive sets of similarities and differences in comparison to human psoriasis. For all five models, correspondence to the human disease was strong with respect to genes involved in epidermal development and keratinization. Immune and inflammation-associated gene expression, in contrast, was more variable between models as compared to the human disease. These findings support the value of all five models as research tools, each with identifiable areas of convergence to and divergence from the human disease. Additionally, the approach used in this paper provides an objective and quantitative method for evaluation of proposed mouse models of psoriasis, which can be strategically applied in future studies to score strengths of mouse phenotypes relative to specific aspects of human psoriasis. Global transcriptional profiling was utilized to evaluate the similarity between human psoriasis and the psoriasis-like phenotypes that develop in five mouse models (K5-Tie2, IMQ, K14-AREG, K5-Stat3C, K5-TGFbeta1)
2011-03-03 | GSE27628 | GEO