Epidermal keratinocytes and IFNg, TNFa and IL1 treatment
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE440 | GEO | 2003/06/24
SECONDARY ACCESSION(S): PRJNA85023
REPOSITORIES: GEO
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Project description:human primay macrophages (hMDMs) were unstimulated, stimulated with IFNg or costimulated with IFNg and TNFa for 18h
2024-08-14 | GSE268354 | GEO
Project description:Epidermal keratinocytes and IFNg, TNFa and IL1 treatment
| PRJNA85023 | ENA
Project description:Cultured epidermal keratinocyte controls used for IFNg, TNFa and IL1 treatment. Interferon (IFN)-gamma, is a multifunctional, immunomodulatory cytokine with cell type-specific antiviral activities, particularly important in skin, where it is implicated in many diseases ranging from warts to psoriasis and cancer. Since epidermis is our first line of defence against many viruses, we investigated the molecular processes regulated by IFN-gamma in keratinocytes using DNA microarrays. We identified the IFN-gamma-regulated keratinocyte-specific genes in keratinocytes, IFN-gamma-induced tight junction proteins, presumably to deny viruses paracellular routes of infection. Furthermore, differing from published data, we find that IFN-gamma suppressed the expression of keratinocytes differentiation markers including desmosomal proteins, cornified envelope components and suprabasal cytokeratins. Inhibition of differentiation may interfere with the epidermal tropism of viruses that require differentiating cells for growth, for example, papillomaviruses. As in other cell types, IFN-gamma induced HLA, cell adhesion and proteasome proteins, facilitating leukocyte attraction and antigen-presentation by keratinocytes. IFN-gamma also induced chemokine/cytokines specific for mononuclear cells. IFN-gamma suppressed the expression of over 100 genes responsible for cell cycle, DNA replication and RNA metabolism, thereby shutting down many nuclear processes and denying viruses a healthy cell in which to replicate. Thus, uniquely in keratinocytes, IFN-gamma initiates a well-organized molecular programme boosting host antiviral defences, obstructing viral entry, suppressing cell proliferation and impeding differentiation.
2007-10-26 | E-GEOD-440 | biostudies-arrayexpress
Project description:NGS5522 - hMDMS response to IFNg and TNFa
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Project description:Interleukin-1 is a proinflammatory and immunomodulatory cytokine that plays a crucial role in inflammatory diseases of the skin, including bacterial infections, bullous diseases, UV damage and especially psoriasis. To characterize the molecular effects of IL-1 in epidermis, we defined the transcriptional changes in human epidermal keratinocytes 1, 4, 24, and 48 h after treatment with IL-1a. IL-1 significantly regulated 388 genes, including genes associated with proteolysis, adhesion, signal transduction, proliferation, and epidermal differentiation. IL-1 induces many genes that have antimicrobial function. Secreted cytokines, chemokines, growth factors, and their receptors are the prominent targets of IL-1 regulation, including IL-8, IL-19, elafin, C3, and S100A proteins, which implicates IL-1 in the pathogenesis of inflammatory diseases. IL-1 induced not only proliferation-associated genes but also differentiation marker genes such as transglutaminase-1 and involucrin, which suggests that IL-1 plays an important role in the aberrant proliferation and differentiation seen in psoriasis. Correlation of IL-1 regulated genes with the TNFa and IFNg regulated ones showed more similarities between IL-1 and TNFa than IL-1 and IFNg, whereas Oncostatin-M affected a largely unrelated set of genes. IL-1 regulates many genes previously shown to be specifically over-expressed in psoriasis. In summary, IL-1 regulates a characteristic set of genes that define its specific contribution to inflammation and aberrant differentiation in skin diseases. Keywords: Time course
2007-09-22 | GSE9120 | GEO
Project description:Interleukin-1 is a proinflammatory and immunomodulatory cytokine that plays a crucial role in inflammatory diseases of the skin, including bacterial infections, bullous diseases, UV damage and especially psoriasis. To characterize the molecular effects of IL-1 in epidermis, we defined the transcriptional changes in human epidermal keratinocytes 1, 4, 24, and 48 h after treatment with IL-1a. IL-1 significantly regulated 388 genes, including genes associated with proteolysis, adhesion, signal transduction, proliferation, and epidermal differentiation. IL-1 induces many genes that have antimicrobial function. Secreted cytokines, chemokines, growth factors, and their receptors are the prominent targets of IL-1 regulation, including IL-8, IL-19, elafin, C3, and S100A proteins, which implicates IL-1 in the pathogenesis of inflammatory diseases. IL-1 induced not only proliferation-associated genes but also differentiation marker genes such as transglutaminase-1 and involucrin, which suggests that IL-1 plays an important role in the aberrant proliferation and differentiation seen in psoriasis. Correlation of IL-1 regulated genes with the TNFa and IFNg regulated ones showed more similarities between IL-1 and TNFa than IL-1 and IFNg, whereas Oncostatin-M affected a largely unrelated set of genes. IL-1 regulates many genes previously shown to be specifically over-expressed in psoriasis. In summary, IL-1 regulates a characteristic set of genes that define its specific contribution to inflammation and aberrant differentiation in skin diseases. Experiment Overall Design: keratinocytes were treated with 25 ng/ml IL-1 and transcriptomes compared to untreated controls at 1, 4, 24 and 48 h post treatment.
2008-06-16 | E-GEOD-9120 | biostudies-arrayexpress
Project description:The psoKC (psoriatic keratinocyte) model is represnting the behavour of keratinocytes in the later or chronic stage of psoriasis in response to the main cytokines that constitute the characteristic cytokine milieu, namely IFNg and TNFa (mainly derived by Th1 cells), and IL-17 and IL-22 (mainly derived by Th17 cells).
Additionally, the model explores the role of exogenous PGE2 through the activation of EP4 receptor signaling. The response to the aforementioned stimuli was not only limited to the cell fate decisions of keratinocytes (proliferation, apoptosis or differentiation) but also include their effect on the psoriatic environment with respect to the secretion of ligands and intercellular-acting stimuli.
2022-12-14 | MODEL2109300001 | BioModels
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:Normal human epidermal keratinocyte mRNA sequencing with LL37 and/or U1 RNA
| PRJNA413273 | ENA
Project description:Epidermal keratinocytes respond to extracellular influences by activating cytoplasmic signal transduction pathways that change the transcriptional profiles of affected cells. To define responses to two such pathways, p38 and ERK, we used SB203580 and PD98059 as specific inhibitors, and identified the regulated genes after 1, 4, 24 and 48 hrs, using Affymetrix’ Hu133Av2 microarrays. Additionally, we compared genes specifically regulated by p38 and ERKs with those regulated by JNK and by all three pathways simultaneously. We find that the p38 pathway induces the expression of extracellular matrix and proliferation-associated genes, while suppressing microtubule-associated genes; the ERK pathway induces the expression of nuclear envelope and mRNA splicing proteins, while suppressing steroid synthesis and mitochondrial energy production enzymes. Both pathways promote epidermal differentiation and induce feedback inactivation of MAPK signaling. c-FOS, SRY and N-Myc appear to be the principal targets of the p38 pathway, Elk-1 SAP1 and HLH2 of ERK, while FREAC-4, ARNT and USF are common to both. The results for the first time comprehensively define the genes regulated by the p38 and ERK pathways in epidermal keratinocytes and suggest a list of targets potentially useful in therapeutic interventions. Human epidermal keratinocytes are grown in Keratinocyte Serum-Free Medium (Gibco) supplemented with 0.05 mg/ml bovine pituitary extract, 2.5 ng/ml epidermal growth factor, 0.09 mM CalCl2 and 1% penicillin/streptomycin (KGM). They are switched to Keratinocyte Serum Free-Media (Gibco) supplemented only with 1% penicillin/streptomycin (KBM) 24 h prior to commencing experiments. A set is left as controls, others treated with 5 uM JNK inhibitor SP600125, 15 uM p38 inhibitor SB203580, or 50 um ERK inhibitor PD98059. Timecourse of treated and parellel control samples over a 48 hr period was performed.
2013-09-05 | E-GEOD-50591 | biostudies-arrayexpress