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Interleukin-4 and interleukin-13 cytokines effect on epidermal keratinocytes

ABSTRACT: Analysis of cultured epidermal keratinocytes treated with interleukin-4 (IL-4) and interleukin-13 (IL-13). IL-4 and IL-13 are up-regulated in atopic dermatitis. Results provide insight into the role of IL-4 and IL-13 cytokines in the pathogenesis of atopic dermatitis. Analysis of epidermal keratinocytes transfected with dual oxidase 1 (DUOX1) siRNA knockdown before treatment with IL-4 and IL-13. DUOX1 is one of the NOX family members of NADPH oxidases whose primary function is ROS generation. Results provide insight into the role of the incraesed expression of DUOX1 in IL-4/IL-13-treated NHEK for IL4/IL13 signaling. IL-4 and IL-13 induced gene expression in human epidermal keratinocytes (NHEK) was measured at 48 hours. Gene expression in NHEK tranfected with 10 nM DUOX1 siRNA followed by treatment with 100 ng/ml IL-4 and 100 ng/ml IL-13 was measured at 48 hours. Three independent experiments were performed using different strains for each experiment.

ORGANISM(S): Homo sapiens

SUBMITTER: Setsuya Aiba

PROVIDER: E-GEOD-20706 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Interleukin-4 and interleukin-13 cytokines effect on epidermal keratinocytes

Project description:Analysis of cultured epidermal keratinocytes treated with interleukin-4 (IL-4) and interleukin-13 (IL-13). IL-4 and IL-13 are up-regulated in atopic dermatitis. Results provide insight into the role of IL-4 and IL-13 cytokines in the pathogenesis of atopic dermatitis. Analysis of epidermal keratinocytes transfected with dual oxidase 1 (DUOX1) siRNA knockdown before treatment with IL-4 and IL-13. DUOX1 is one of the NOX family members of NADPH oxidases whose primary function is ROS generation. Results provide insight into the role of the incraesed expression of DUOX1 in IL-4/IL-13-treated NHEK for IL4/IL13 signaling.

2010-10-31 | GSE20706 | GEO

recombinant human epidermal model LC-MS/MS

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2023-08-07 | PXD043085 | Pride

Profiling of genes expressed in cultured human keratinocytes established from the bulge region of hair follicles.

Project description:We established a culture method of human keratinocytes from the bulge region of a plucked hair follicle, that contains multipotent epithelial stem cells with high proliferative potential. Using our method, keratinocyte cultures were successfully obtained from all subjects without invasive skin biopsies. We compared the gene expression profiles between the cultured keratinocytes derived from human hair-follicle-bulge (bulgeM-bM-^@M-^Sderived keratinocytes; BDKs) and neonatal human epidermal keratinocytes (NHEKs), and between BDKs from donors with atopic dermatitis and non-atopic controls using microarray analysis. Keywords: expressin profiling Two cell cultures, BDK vs. NHEK cells. 18 BDKs; derived from eighteen healthy volunteers , 6 NHEKs; purchased from Kurabo (Osaka, Japan). One replicate per array.

2013-02-05 | E-GEOD-13709 | biostudies-arrayexpress

Type 2 cytokine-dependent skin barrier regulation in personalized 2D- and 3D skin models of atopic dermatitis: A pilot study

Project description:Keratinocytes from healthy donors stimulated with type 2 cytokines are often used to experimentally study atopic dermatitis (AD) inflammatory responses. Due to potential intrinsic alterations, it seems favorable to use keratinocytes from AD patients. Keratinocytes isolated from hair follicles offer a non-invasive approach to investigate AD-derived keratinocytes. To evaluate whether such AD-derived keratinocytes are suitable to mimic AD inflammatory responses we compared hair follicle-derived keratinocytes from healthy donors and AD patients in a type 2 cytokine environment. Stimulation of AD-derived keratinocytes with IL-4 and IL-13 induced higher expression changes of AD-associated markers as compared to healthy keratinocytes. The combination of IL-4 and IL-13 generally induced highest expression changes, but IL-13 alone also induced significant changes of AD-specific markers. Similar to the 2D cultures, IL-4/IL-13 stimulation of 3D skin models generated with AD-derived keratinocytes modulated the expression of several AD-relevant factors. Whole transcriptome analysis revealed that IL-4 and IL-13 acted similarly on these 3D skin models. Histologically, IL-13 alone and in combination with IL-4 increased epidermal spongiosis, a histological hallmark of AD skin. Taken together, our pilot study suggests that hair follicle-derived keratinocytes from AD patients represent a useful model system to study AD-related inflammation in a personalized in vitro model.

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Gene expression changes by 2,4-dinitrochlorobenzene in human bulge-derived keratinocytes

Project description:In the epidermis, keratinocytes are involved in physical and first-line immune protection of the host. In this work, we analyzed molecular responses after the addition of contact sensitizers, 2,4-dinitrochlorobenzene (DNCB) using cultured human keratinocytes from the bulge region of a plucked hair follicle (bulge-derived keratinocytes; BDKs) in comparison with neonatal human epidermal keratinocytes NHEK and human monocytic leukemia THP-1. The changes in gene expression by the treatment of DNCB in BDKs were different from those in THP-1. Many genes orchestrating keratinocyte differentiation, which interact TGF-Î² and BMP signaling pathway, were significantly up-regulated in response to DNCB. Keywords: Comparison analysis of gene expression changes by the treatment of DNCB three cell strains composed of four samples; two BDKs established from different donors, NHEK, and THP-1. One replicate per array.

2010-04-09 | E-GEOD-14838 | biostudies-arrayexpress

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2015-08-27 | E-GEOD-66359 | biostudies-arrayexpress

Genome-wide analysis of keratinocyte gene expression during their course of differentiation in presence or absence of JNK1,2-deficient or wildtype immortalized mouse embryonic fibroblasts (MEFs)

Project description:Analysis of keratinocyte differentiation in presence or absence of fibroblast-derived JNK-dependent soluble factors in vitro. The hypothesis tested in the present study was that JNK-dependent fibroblast-derived soluble factors promote an efficient keratinocyte differentiation. Results provide important information about reduced expression of a subset of differentiation associated genes in keratinocytes in the absence of JNK-dependent fibroblast-derived soluble factors. In vitro transwell co-culture experiments were performed using jnk1-/-jnk2-/- or wildtype immortalized mouse embryonic fibroblasts (MEFs) and differentiating primary normal human epidermal keratinocytes (NHEK) over a time course of 6 days. Total RNA was obtained from NHEK prior to cultivation with MEFs (day 0) and every second day (days 2, 4, and 6) during co-culture. MEFs have been described previously in Sabapathy et al. (2004) Mol Cell 15:713-25.

2013-11-26 | E-GEOD-48613 | biostudies-arrayexpress

Proteomic analysis of small extracellular vesicles (sEVs) derived from primary keratinocytes cultured in different calcium concentrations, treated with a peanut allergen extract and atopic dermatitis (AD)-relevant cytokines

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TWEAK mediates inflammation in experimental atopic dermatitis and psoriasis

Project description:Atopic dermatitis and psoriasis are driven by alternate type 2 and type 17 immune responses, but some proteins might be critical to both diseases. We show that a deficiency of the TNF superfamily molecule TWEAK (TNFSF12) in mice results in defective maintenance of atopic dermatitis-specific Th2 and psoriasis-specific Th17 cells in the skin, and impaired expression of disease-characteristic chemokines and cytokines, such as CCL17 and TSLP in atopic dermatitis, and CCL20 and IL-19 in psoriasis. The TWEAK receptor, Fn14, is upregulated in keratinocytes and dermal fibroblasts, and TWEAK induces these cytokines and chemokines alone and in synergy with the signature T helper cytokines of either disease, IL-13 and IL-17. Furthermore, subcutaneous injection of recombinant TWEAK into naïve mice induces cutaneous inflammation with histological and molecular signs of both diseases. TWEAK is therefore a critical contributor to skin inflammation and a possible therapeutic target in atopic dermatitis and psoriasis.

2017-05-01 | GSE96957 | GEO

AhR links air pollution and atopic dermatitis via Artemin induction

Project description:Atopic dermatitis is increasing worldwide, correlating with air pollutions. Various organic components of pollutants activate transcription factor AhR (aryl-hydrocarbon receptor). We have established AhR-CA mice, whose keratinocytes express constitutive-active AhR, and these mice developed atopic dermatitis-like frequent scratching and allergic inflammation. In this study we performed ChIP-seq analyses and identified keratinocyte-specific AhR target genes, including inflammatory cytokines Tslp and IL33, and neurotrophic factor Artemin. While AhR-CA mice exhibited epidermal hyperinnervation and alloknesis leading to hypersensitivity to pruritus, blockade of Artemin alleviated these phenotypes. AhR-CA mice showed scratching-induced barrier insufficiency and enhanced sensitization to epicutaneously-applied antigens, recapitulating human atopic dermatitis. Consistently, AhR activation and Artemin expression was detected in the epidermis of atopic dermatitis patients and keratinocytes exposed to air pollutants. Thus, AhR in keratinocytes senses the environmental stimuli and responds to them through moderating inflammation. We propose a mechanism in which air pollution induces atopic dermatitis through AhR activation.

2016-11-13 | GSE72449 | GEO

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