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IL-22 down-regulates filaggrin expression and affects expression of profilaggrin processing enzymes by keratinocytes

ABSTRACT: Genome-wide analysis of gene expression after stimulation with cytokines to assess the main processes, molecular functions and cellular components affected as well as genes related to skin barrier function.

ORGANISM(S): Homo sapiens

PROVIDER: GSE28158 | GEO | 2011/12/30

SECONDARY ACCESSION(S): PRJNA139677

REPOSITORIES: GEO

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IL-22 down-regulates filaggrin expression and affects expression of profilaggrin processing enzymes by keratinocytes

Project description:Genome-wide analysis of gene expression after stimulation with cytokines to assess the main processes, molecular functions and cellular components affected as well as genes related to skin barrier function. HaCaT cells were exposed to IL-22 (200ng/ml) for 12h. The cells were lysed, total RNA was extracted and microarray study was performed on Illumina HT12 platform.

2011-12-30 | E-GEOD-28158 | biostudies-arrayexpress

Gene expression profile of human epidermal keratinocytes in response to IFNgamma, IL-4, IL-6, IL-17A and IL-22

Project description:To understand the role of epidermal keratinocytes in immunopathology of skin diseases with predominant T helper (Th) cell responses, we measured the genome-wide transcriptional profile of human keratinocytes in response to IFNgamma, IL-4, IL-17A or IL-22, major cytokines produced by Th1, Th2, Th17 or Th22 cells, respectively. IL-6 was also included in the transcriptional profile analysis because a variety of pro-inflammatory stimuli stimulate human keratinocytes to produce IL-6 that has an autocrine or paracrine role in epidermal immunity. We aimed to discover commonly expressed genes in human keratinocytes in response to pro-inflammatory cytokines, which would be associated with common pathophysiological responses in various skin diseases such as skin permeability barrier disruption or epidermal hyperplasia. Normal human keratinocytes (NHKs) were stimulated with IFNγ, IL-4, IL-6, IL-17A and IL-22 for 24 hours and harvested for total RNA extraction and hybridization on Affymetrix microarrays.

2014-10-02 | E-GEOD-53751 | biostudies-arrayexpress

IL-17 downregulates filaggrin and affects epidermal barrier function gene expression; potential role in the pathogenesis of atopic eczema

Project description:Genome-wide analysis of gene expression after stimulation with cytokines to assess the main processes, molecular functions and cellular components affected as well as genes related to skin barrier function. HaCaT cells were exposed to IL-17A (200ng/ml) for 12h. The cells were lysed, total RNA was extracted and microarray study was performed on Illumina HT12 platform.

2012-11-01 | E-GEOD-27533 | biostudies-arrayexpress

IL-17 downregulates filaggrin and affects epidermal barrier function gene expression; potential role in the pathogenesis of atopic eczema

2012-11-01 | GSE27533 | GEO

The crosstalk between IL-22 signaling and miR-197 in human keratinocytes.

Project description:The interaction between the immune system and epithelial cells is tightly regulated. Aberrations of this balance may result in inflammatory diseases such as psoriasis, inflammatory bowel disease and rheumatoid arthritis. IL-22 is produced by Th17, Th22 and Th1 cells. Putative targets for IL-22 are cells in the skin, kidney, digestive and respiratory systems. The highest expression of IL-22 receptor is found in the skin. IL-22 plays an important role in the pathogenesis of T cell-mediated inflammatory diseases such as psoriasis, inflammatory bowel disease and rheumatoid arthritis. Recently, we found that miR-197 is down regulated in psoriatic lesions. In the present work we show that miR-197 over expression inhibits keratinocytes proliferation induced by IL-22 and keratinocytes migration. In addition, we found that IL-22 activates miR-197 expression through the binding of phosphorylated STAT3 to sequences in the putative promoter of miR-197. Finally we found that IL-22 receptor subunit IL22RA1 is a direct target of miR-197. Hence, we identified a novel feedback loop controlling IL-22 signaling, in which IL-22 induces miR-197, which in turn, negatively regulates IL-22 receptor and attenuates the biological outcome of such signaling. Regulation of this pathway may be important in inflammatory skin disorders such a psoriasis and in wound healing.

| S-EPMC4160297 | biostudies-literature

Effect of histamine on human keratinocytes

2013-12-01 | GSE41585 | GEO

Effect of histamine on human keratinocytes

Project description:Genome-wide analysis of gene expression after stimulation with histamine to assess the main processes, molecular functions and cellular components affected as well as genes related to skin barrier function. HaCaT cells were exposed to histamine (1ug/ml) for 24h. The cells were lysed, total RNA was extracted and microarray study was performed on Illumina HT12 platform.

2013-12-01 | E-GEOD-41585 | biostudies-arrayexpress

IL-22 promotes postnatal formation of MUC17 glycocalyx barrier that protects host enterocytes

Project description:The apical aspects of absorptive epithelial cells form a highly organized brush border membrane (BBM), shaped by densely packed microvilli that are coated with a glycocalyx. Here, we present evidence showing that the glycocalyx forms an epithelial barrier that prevents exogenous molecules from gaining access to the BBM. We used a multiomics approach to investigate function and regulation of membrane mucins exposed on the enterocytic BBM during postnatal development of the small intestine. Muc17 was identified as a major membrane mucinin the glycocalyx that was specifically upregulated by IL-22 as part of an epithelial defense repertoire during suckling-weaning transition. High levels of IL-22 at the time of weaning primed progenitor enterocyte to express Muc17 as they migrate out of intestinal crypts to replace neonatal enterocytes. Our findings propose a role for membrane mucin Muc17 in epithelial barrier function in the small intestine.

2021-02-16 | PXD018592 | Pride

CD28 Autonomous Signaling Orchestrates IL-22 Expression and IL-22-Regulated Epithelial Barrier Functions in Human T Lymphocytes.

Project description:IL-22 is a member of the IL-10 cytokine family involved in host protection against extracellular pathogens, by promoting epithelial cell regeneration and barrier functions. Dysregulation of IL-22 production has also frequently been observed in acute respiratory distress syndrome (ARDS) and several chronic inflammatory and autoimmune diseases. We have previously described that human CD28, a crucial co-stimulatory receptor necessary for full T cell activation, is also able to act as a TCR independent signaling receptor and to induce the expression of IL-17A and inflammatory cytokines related to Th17 cells, which together with Th22 cells represent the main cellular source of IL-22. Here we characterized the role of CD28 autonomous signaling in regulating IL-22 expression in human CD4+ T cells. We show that CD28 stimulation in the absence of TCR strongly up-regulates IL-22 gene expression and secretion. As recently observed for IL-17A, we also found that CD28-mediated regulation of IL-22 transcription requires the cooperative activities of both IL-6-activated STAT3 and RelA/NF-κB transcription factors. CD28-mediated IL-22 production also promotes the barrier functions of epithelial cells by inducing mucin and metalloproteases expression. Finally, by using specific inhibitory drugs, we also identified CD28-associated class 1A phosphatidylinositol 3-kinase (PI3K) as a pivotal mediator of CD28-mediated IL-22 expression and IL-22-dependent epithelial cell barrier functions.

| S-EPMC7592429 | biostudies-literature

Expression data from keratinocytes treated either with IL-22 or combination of tofacitinib (JAK1/3 inhibitor) and IL-22 at 6 hours

Project description:JAK inhibitors like tofacitinib were thought to act primarily on T cells. However, our data and recent research suggest that JAK receptors are also present on keratinocytes. Here, we show effect of tofacitinib on primary keratinocytes, which could explain effects of topical tofacitinib treatment in psoriasis. We have performed whole transcriptome analysis (using microarray) on RNA isolated from cultured primary keratinocytes treated either with IL-22 alone or combination of tofacitinb and IL-22 at 6 hours

2017-10-03 | GSE104509 | GEO

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