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Staphylococcus Aureus and Streptococcus Pyogenes Induce Psoriasis-Related Transcriptomes in Human Keratinocytes Augmented by IL-17A and TNF-α

ABSTRACT: This study aims to define the interactions that SA or SP may have with IL-17A and TNF-α in human keratinocytes, as well as the similarity to psoriasis vulgaris

ORGANISM(S): Homo sapiens

PROVIDER: GSE207390 | GEO | 2023/03/24

REPOSITORIES: GEO

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Staphylococcus Aureus and Streptococcus Pyogenes Induce Psoriasis-Related Transcriptomes Augmented by IL-17A and TNF-α.

Project description: Not available

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IL-17A plays a central role in the expression of psoriasis signature genes through induction of IkappaB-zeta in keratinocytes

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

IL-17A and TNF-α inhibitors induce multiple molecules andsignal pathway change in psoriasis

Project description:Adalimumab and secukinumab are commonly used for moderate-severe psoriasis vulgaris (PV), but distinct individual response and impaired effectiveness happen occasionally. Little is known about it. Here, we report a proteomic analysis of psoriatic lesions from patients treated with these drugs using Data Independent Acquisition Mass Spectrometry (DIA-MS). Thousands of differentially expressed proteins (DEPs) changed over 12 weeks of treatment. Network analysis showed DEPs could interact and induce transformation in matrix components, metabolic regulation, and immune response. PRM analysis suggested S100s, STAT1, KRT2, TYMP, SOD2, HSP90AB1, TFRC, and COL5A1 were the most significantly changed proteins in both groups. There is a positively association between the psoriasis area and severity index (PASI) score and three proteins (TFRC, IMPDH2, KRT2). Our study suggests that inhibition of IL-17A and TNF-α can induce multiple molecules change in psoriatic lesions and overlapping effect on immune response and proces

2022-10-20 | PXD037579 |

Staphylococcus Aureus and Streptococcus Pyogenes Induce Psoriasis-Related Transcriptomes in Human Keratinocytes Augmented by IL-17A and TNF-α

Project description:Staphylococcus Aureus and Streptococcus Pyogenes Induce Psoriasis-Related Transcriptomes in Human Keratinocytes Augmented by IL-17A and TNF-α

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IL-17A plays a central role in the expression of psoriasis signature genes through induction of IkappaB-zeta in keratinocytes

2016-03-08 | GSE77719 | GEO

Double-negative T cells ameliorate psoriasis by selectively inhibition on IL-17A producing γδ T cells

Project description:Psoriasis is a chronic immune-mediated skin condition influenced by genetics and environmental factors. γδ T cells, as the main sources of IL-17A, play pivotal roles in the inflammatory processes of psoriasis. During psoriasis pathogenesis, inhibiting the secretion of IL-17A has emerged as a novel therapeutic approach for treating psoriasis. Double-negative T (DNT) cells is a novel type of immunosuppressive cells. Our preliminary research has unveiled that DNT cells play a significant immunoregulatory role in autoimmune and allergic diseases. In this study, we aimed to evaluate the protection of DNT cells and explore its underlying mechanism.

2024-04-10 | GSE248626 | GEO

Single-cell genomics segregate different transcriptomic impacts of anti-IL-17A blockade on type 17 T-cells and regulatory immune cells in psoriasis skin

Project description:Durable psoriasis improvement has been reported in a subset of psoriasis patients after treatment withdrawal of biologics blocking IL-23/Type 17 T-cell (T17) autoimmune axis. However, it is not well understood if systemic blockade of the IL-23/T17 axis promotes immune tolerance in psoriasis skin. The purpose of the study was to find translational evidence that systemic IL-17A blockade promotes regulatory transcriptome modification in human psoriasis skin immune cell subsets. We analyzed human psoriasis lesional skin 6 mm punch biopsy tissues before and after systemic IL-17A blockade using the muti-genomics approach integrating immune cell-enriched scRNA-seq (n = 18), microarray (n = 61), and immunohistochemistry (n = 61) with repository normal control skin immune cell-enriched scRNA-seq (n = 10) and microarray (n = 8) data. For the T17 axis transcriptome, systemic IL-17A blockade depleted 100% of IL17A + T-cells and 95% of IL17F + T-cells in psoriasis skin. The expression of IL23A in DC subsets was also downregulated by IL-17A blockade. The expression of IL-17-driven inflammatory mediators (IL36G, S100A8, DEFB4A, and DEFB4B) in suprabasal keratinocytes was correlated with psoriasis severity and was downregulated by IL-17A blockade. For the regulatory DC transcriptome, the proportion of regulatory semimature DCs expressing regulatory DC markers of BDCA-3 (THBD) and DCIR (CLEC4A) was increased in posttreatment psoriasis lesional skin compared to pretreatment psoriasis lesional skin. In addition, IL-17A blockade induced higher expression of CD1C and CD14, which are markers of CD1c+ CD14+ dendritic cell (DC) subset that suppresses antigen-specific T-cell responses, in posttreatment regulatory semimature DCs compared to pretreatment regulatory semimature DCs. In conclusion, systemic IL-17A inhibition not only blocks the entire IL-23/T17 cell axis but also promotes regulatory gene expression in regulatory DCs in human psoriasis skin.

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Interleukin-17A based dysregulation of Human Primary Keratinocyte proteome

Project description:To delineate mechanisms for psoriasis pathogenesis driven by the interleukin-17A, proteomic dysregulations were studied in a Human Primary Keratinocyte model system. Label-free quantification was performed and fold-changes were obtained for abundances of proteins in IL-17A treated keratinocytes versus those from IL-17A treated keratinocytes. Briefly, Human Primary Keratinocytes were isolated and treated with the cytokine IL-17A (50ng/ml) in incomplete media devoid of any growth factors. Tryptic digested and desalted peptide samples were injected in Thermoscientific Q-Exactive Plus instruments through EasyNLC HPLC autosampler. The instruments were set to MS1 resolution of 70000 and MS2 resolution of 17500. The acquisition experiments were optimized to run on 120 min gradients. The MS spectra were analyzed using the Thermoscientific mass informatics platform Proteome discoverer version 2.2. The common workflows for discovery proteomics were used with Mascot and SequestHT as search engines. This dataset helped to simulate the IL-17A-driven inflammation in keratinocytes and uncovered many putative druggable targets in the context of psoriasis.

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IL-36 and IL-17A Cooperatively Induce a Psoriasis-like Gene Expression Response in Human Keratinocytes

Project description:In this study we tested interactions between IL-36 and IL-17A in human keratinocytes. 24 hours of IL-36 stimulation in keratinocytes promoted IL-36, IL-17C, and characteristic psoriasis-related molecule expressions in normal human epidermal keratinocytes in dose-dependent manners as measured by mRNA and protein quantification.

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ncRNA expression profile in keratinocytes of patients with psoriasis vulgaris

Project description:The aim of our study was to explore lncRNA expression profile in keratinocytes of patients with psoriasis vulgaris to provide new insights into psoriasis.

2023-02-28 | GSE146149 | GEO