Alloferon and IL-22 receptor expression regulation on the pathogenesis of imiquimod-induced psoriasis
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PROVIDER: PRJNA1205354 | ENA |
REPOSITORIES: ENA
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Project description:We investigated the regulatory role of alloferon in the development of psoriasis in an imiquimod (IMQ)-induced psoriasis model through the regulation of IL-22Rα expression. Psoriasis is an immune-mediated inflammatory skin disease. IL-22, a proinflammatory cytokine, is implicated in psoriasis pathogenesis; however, there is currently no established biological treatment targeting IL-22 or its receptor, IL-22Rα. Alloferon is a short peptide that has an anti inflammatory effect on skin disorders; however, little is known about its anti-inflammatory activity in psoriasis. This study demonstrate that alloferon could be an effective potential drug for the treatment of psoriasis by interrupting IL-22 signaling and factors related to skin inflammation.
2025-03-05 | GSE285640 | GEO
Project description:Psoriasis is an inflammatory skin disease and the exact pathogenesis has not been fully illuminated yet. It has been demonstrated that interleukin-22 (IL-22) plays a significant role in the pathogenesis of psoriasis. Our study aimed to explore the role of IL-22 and its target miRNAs in pathogenesis of psoriasis.
2015-08-27 | GSE72396 | GEO
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: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: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.
2017-10-06 | GSE104603 | GEO
Project description:Psoriasis vulgaris is a chronic inflammatory skin disease which tends to affect the extensor surface of the body. IL-17A and IL-23 antagonists are currently the main and powerful therapeutic choices but the skin areas which are subject to stretching, namely knees, elbows and the lower back, are often reluctant to treatments. ; Hence, we hypothesize that stretching has a dominant effect on psoriasis development. First, we found that, in imiquimod-treated psoriasis-like mouse model, mechanical stretch promotes a significant increase in clinical severity, epidermal thickness, and inflammatory cell infiltration of psoriasis. Transcriptomics profiling revealed that Il6 and Il1b genes are significantly upregulated and play a major role in the activation and recruitment of neutrophils, macrophages, and T cells in stretching group. Upstream analysis further identifies NF-κB as a critical transcription factor to drive pro-inflammatory cytokine expression during stretch application. Immunofluorescence staining confirmed the increased expression of IL-1β and IL-6. In summary, our findings uncover that the mechanical biology contributes to psoriasis progression mainly through enhancing the production of IL-1β and IL-6.
2024-07-29 | GSE218745 | GEO
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.
2023-06-15 | GSE152637 | 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:In psoriasis lesions, a diverse mixture of cytokines is upregulated which influence each other generating a complex inflammatory situation. Although this is the case, the inhibition of Interleukin-17A (IL-17A) alone showed unprecedented clinical results in patients, indicating that IL-17A is a critical inducer of psoriasis pathogenesis. To elucidate IL-17A-driven keratinocyte-intrinsic signaling pathways, we treated monolayers of normal human epidermal keratinocytes in vitro with a mixture of 6 cytokines (IL-17A, TNF-a, IL-17C, IL-22, IL-36g and IFN-g) involved in psoriasis, to mimic the inflammatory milieu in psoriasis lesions. Microarray and gene set enrichment analysis revealed that this cytokine mixture induced similar gene expression changes with the previous transcriptome studies using psoriasis lesions. Importantly, we identified a set of IL-17A-regulated genes in keratinocytes, which recapitulate typical psoriasis genes exemplified by DEFB4A, S100A7, IL19 and CSF3, based on differences in the expression profiles of cells stimulated with 6 cytokines versus cells stimulated with only 5 cytokines lacking IL-17A. Furthermore a specific IL-17A-induced gene, NFKBIZ, which encodes IkappaB-zeta, a transcriptional regulator for NF-kappaB, was demonstrated to have a significant role for IL-17A-induced gene expression. Thus, we present novel in vitro data from normal human keratinocytes that would help elucidating the IL-17A-driven keratinocyte activation in psoriasis. Cytokine mixture-induced gene expression in primary normal human epidermal keratinocytes (NHEKs) was measured at 24 hours after exposure. NHEKs were exposed to the combination of selected six cytokines (IL-17A: 100 ng/ml, TNF-a: 10 ng/ml, IFN-g: 10 ng/ml, IL-17C: 100 ng/ml, IL-22: 100 ng/ml, IL-36g: 500 ng/ml) , or to the different combinations of five of the six cytokines (in total, 7 different treatments and one untreated control). No replicate experiments were conducted.
2016-03-08 | E-GEOD-77719 | biostudies-arrayexpress
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.
2024-05-03 | GSE266043 | GEO