Transcriptome analysis of the potential mechanism of Longkui Yinxiao soup in the treatment of imiquimod-induced psoriasis-like mice
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE226452 | GEO | 2023/03/03
REPOSITORIES: GEO
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Project description:Psoriasis is a chronic inflammatory skin disorder that is predominantly characterized by sharply demarcated chronic erythematous plaques. Although its etiological mechanisms are largely unknown, recent evidence suggests that the topical application of imiquimod (IMQ) cream causes psoriasis-like skin inflammation in humans and mice. Skin examined 4 hours after IMQ cream treatment. Results provide insight into the role of each knockout mice phenotype in the response to IMQ-induced psoriasis model.
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Project description:The mechanisms underlying pruritus of imiquimod (IMQ)-induced psoriasis remain poorly understood. In this study, we investigated whether there are certain key signaling molecules downstream of the recently identified peptides mediating itch in the spinal cord. We investigated the changes in the trascriptome by performing RNAseq of cervical spinal cords in control and IMQ-induced psoriasis. Our study represents the detailed analysis of transcriptomes of spinal cord in chronic itch model with biologic replicates, generated by RNA-seq technology.
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Project description:Expression data from Imiquimod-induced psoriasis mouse model
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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.
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Project description:Patients with psoriasis are at a higher risk of developing nonalcoholic fatty liver disease. We previously identified an oxidized derivative of cholesterol, 7-ketocholesterol (7KC), in diet-induced steatohepatitic mice. Here, we investigated whether 7KC exacerbates psoriasis-like dermatitis by accelerating steatohepatitis in mice. A high fat/high cholesterol/high sucrose/bile salt diet (NASH diet) with or without 0.0125% 7KC was fed to C57BL/6 mice (7KC or control group) for three weeks to induce steatohepatitis. 5% imiquimod cream was then applied to the ears and dorsal skin for four days to induce psoriasis-like dermatitis. Hepatic lipid accumulation and inflammatory cell infiltration were exacerbated in the 7KC group compared with the control group after three weeks. Serum tumor necrosis factor-α (TNF-α) levels were also elevated in the 7KC group (108.5±9.8 vs. 83.1±13.1 pg/ml, p<0.005). Imiquimod cream increased the psoriasis area severity index (PASI) score in mice in the 7KC group (9.14±0.75 vs. 5.17±1.17, p<0.0001). Additionally, Tnfa, Il23a, Il17a, and Il22 mRNA levels in the dorsal lesion were significantly upregulated. Finally, Th17 cell differentiation and the TNF signaling pathway were enhanced in the dorsal lesions and liver of mice in the 7KC group. These data suggest that steatohepatitis and psoriasis are linked by a potent, diet-related factor.
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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
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Project description:Patients with psoriasis are at a higher risk of developing nonalcoholic fatty liver disease. We previously identified an oxidized derivative of cholesterol, 7-ketocholesterol (7KC), in diet-induced steatohepatitic mice. Here, we investigated whether 7KC exacerbates psoriasis-like dermatitis by accelerating steatohepatitis in mice. A high fat/high cholesterol/high sucrose/bile salt diet (NASH diet) with or without 0.0125% 7KC was fed to C57BL/6 mice (7KC or control group) for three weeks to induce steatohepatitis. 5% imiquimod cream was then applied to the ears and dorsal skin for four days to induce psoriasis-like dermatitis. Hepatic lipid accumulation and inflammatory cell infiltration were exacerbated in the 7KC group compared with the control group after three weeks. Serum tumor necrosis factor-α (TNF-α) levels were also elevated in the 7KC group (108.5±9.8 vs. 83.1±13.1 pg/ml, p<0.005). Imiquimod cream increased the psoriasis area severity index (PASI) score in mice in the 7KC group (9.14±0.75 vs. 5.17±1.17, p<0.0001). Additionally, Tnfa, Il23a, Il17a, and Il22 mRNA levels in the dorsal lesion were significantly upregulated. Finally, Th17 cell differentiation and the TNF signaling pathway were enhanced in the dorsal lesions and liver of mice in the 7KC group. These data suggest that steatohepatitis and psoriasis are linked by a potent, diet-related factor.
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Project description:Crosstalk between keratin-forming cells and aberrant immune cells due to immune imbalance is a key factor in the pathogenesis of psoriasis. Most of the current clinical treatments provide rapid symptomatic relief but bring side effects that should not be ignored. Tetrastigma hemsleyanum polysaccharides (THP) have significant immunomodulatory and anti-inflammatory properties. In this study, we used imiquimod (IMQ)-induced psoriasis mouse model and LPS/IL-6-stimulated HaCaT cell model. The potential and mechanism of action of THP for psoriasis treatment were assessed by Psoriasis Area Severity Index (PASI) score, histopathology, flow cytometry, Western blot, and reverse transcription-polymerase chain reaction. The signs and symptoms of psoriatic mice induced by IMQ were significantly relieved by percutaneous administration of THP, including the improvement of psoriatic skin signs (erythema, folds, scales), pathological changes, decreased PASI score, and decreased spleen index. Results of in vivo and in vitro studies suggest that THP inhibits abnormal cell proliferation and excessive inflammation at skin lesions, balances Th17 immune cells, and blocks the keratinocyte-Th17 cell cycle, thus playing a role in psoriasis treatment by a mechanism that may be related to the regulation of the JAK/STAT3 signaling pathway.
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Project description:We provide a new psoriasis mouse model which is induced by p38 activation in skin. We compared the individual transcriptomic profiles of anisomycin and imiquimod-induced dermatitis. We used microarrays to compare the gene expression pattern between anisomycin- and imiquimod- induced dermatitis.
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