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Comparison of the Inflammatory Circuits in Psoriasis Vulgaris, Non-Pustular Palmoplantar Psoriasis, and Palmo-Plantar Pustular Psoriasis

ABSTRACT: In this study, our aim was to investigate the potential inflammatory pathways underlining PV, PPPP, and NPPP, through histologic and immunohistochemical characterization of the inflammation and gene expression profiling in skin samples of participants with PPPP, NPPP, PV (without palmo-plantar involvement), and healthy controls.

ORGANISM(S): Homo sapiens

PROVIDER: GSE203415 | GEO | 2022/05/25

REPOSITORIES: GEO

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Comparison of the Inflammatory Circuits in Psoriasis Vulgaris, Non-Pustular Palmoplantar Psoriasis, and Palmo-Plantar Pustular Psoriasis

Project description:Comparison of the Inflammatory Circuits in Psoriasis Vulgaris, Non-Pustular Palmoplantar Psoriasis, and Palmo-Plantar Pustular Psoriasis

| PRJNA839789 | ENA

Comparison of healthy, plaque psoriasis and pustular psoriasis FFPE skin biopsies

Project description:Generalized pustular psoriasis (GPP) is a rare, debilitating, and often life-threatening inflammatory disease characterized by episodic infiltration of neutrophils into the skin, pustule development, and systemic inflammation, which can manifest in the presence or absence of chronic plaque psoriasis (PV). Current treatments are unsatisfactory thus a better understanding the pathogenesis of GPP is warranted. To assess the pathophysiological differences between GPP and PV we performed a gene expression study on formalin-fixed paraffin-embedded biopsies of GPP (n=30) and PV (n=12) lesions and healthy control (n=20) skin. Compared with healthy skin, GPP lesions yielded 365 and PV 898 differentially expressed genes respectively, with 190 upregulated in both diseases. We detected higher expression of IL-1 and IL-36 cytokines in GPP lesions compared with PV, and this occurred proximal to neutrophils. We show both activated neutrophils and isolated neutrophil proteases can activate IL-36. Diverging from the Th1/Th17 pathophysiology of PV, significantly fewer IL23A, IL17A, IFNG, CXCL9, CXCL10 and MX1 transcripts were detected in GPP lesions. Our data indicate a level of sustained activation of IL-1 and IL-36 in GPP, inducing neutrophil chemokine expression, infiltration and pustule formation, suggesting that the IL-1 and IL-36 inflammatory axes are the main drivers of disease pathology in GPP.

2017-01-27 | GSE79704 | GEO

Based on Molecular Profiling of Gene Expression, Palmoplantar Pustulosis and Palmoplantar Pustular Psoriasis are Highly Related Diseases that Appear to Be Distinct from Psoriasis Vulgaris

Project description:There is a controversy surrounding the existence of palmoplantar pustulosis (PPP) and palmoplantar pustular psoriasis (PPPP) as separate clinical entities or as variants of the same clinical entity. We used gene expression microarray to compare gene expression in PPP and PPPP. PPP and PPPP could not be differentiated using gene expression microarray suggesting that they are not distinct clinical entities. Increased expression of GPRIN1, and ADAM23 in keratinocytes suggests that these proteins could be new therapeutic targets for PPP/PPPP. Skin biopsies from subjects with PPP (3), PPPP (6), psoriasis vulgaris (10) and acral skin from normal subjects (7) were analyzed using gene expression microarray. Principal component analysis showed that PPP and PPPP were different from psoriasis vulgaris and normal acral skin. However gene expression of PPP and PPPP clustered together and could not be used to differentiate PPP from PPPP. Gene-wise comparison between PPP and PPPP found no gene to be differentially expressed with a false discovery rate lower than 0.6. Surprisingly we found a higher expression of several genes involved in neural pathways (e.g. GPRIN and ADAM23) in PPP/PPPP as compared to psoriasis vulgaris and normal acral skin. Immunohistochemistry confirmed those findings and showed a keratinocyte localization for those proteins.

2016-06-30 | E-GEOD-80047 | biostudies-arrayexpress

Based on Molecular Profiling of Gene Expression, Palmoplantar Pustulosis and Palmoplantar Pustular Psoriasis are Highly Related Diseases that Appear to Be Distinct from Psoriasis Vulgaris

2016-06-30 | GSE80047 | GEO

Pustular Palmoplantar Psoriasis Successfully Treated with Nb-UVB Monochromatic Excimer Light: A Case-Report.

Project description:Barber's palmoplantar pustulosis (PPP) is a form of localised pustular psoriasis, affecting the palmar and plantar surfaces. It is a chronic disease, with a deep impact on the patients' quality of life. The Authors discuss a case of Baber Psoriasis successfully treated with monochromatic excimer light.

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Lack of association between mutation in IL36RN and palmoplantar pustular psoriasis in Chinese patients.

Project description:BackgroundPalmoplantar pustulosis is considered to be a localized pustular psoriasis confined to the palms and soles. Mutation of the IL36RN gene, encoding interleukin-36 receptor antagonist (IL-36Ra), is associated with generalized pustular psoriasis, but IL36RN mutations in Chinese palmoplantar pustulosis patients have not previously been investigated.ObjectiveThe aim of this study was to evaluate the mutation of IL36RN in Chinese patients with palmoplantar pustulosis.MethodsFifty-one Han Chinese patients with palmoplantar pustulosis were recruited. All exons and exon-intron boundary sequences of IL36RN were amplified in polymerase chain reactions, and Sanger sequencing of the amplicons was performed.ResultsAmong the 51 palmoplantar pustulosis patients, four different single-base substitutions were identified in nine patients. The mutations were c.140A>G/p.Asn47Ser in five patients, c.258G>A/p.Met86IIe in two patients, and c.115+6T>C and c.169G>A/p.Val57IIe in one patient each. All mutations were heterozygous. Comparison with the human genome database and reported literature suggested that these variants may not be pathogenic mutations causing palmoplantar pustulosis. Furthermore, there was no difference in disease severity, onset age, or disease duration between patients with these heterozygous IL36RN variants and those without (p>0.1).Study limitationLack of the further evaluation of IL36Ra protein in palmoplantar pustulosis lesions.ConclusionsThe four variants of IL36RN identified did not appear to be associated with the specific phenotypes of palmoplantar pustulosis.

| S-EPMC6939190 | biostudies-literature

Variant analysis of CARD14 in a Chinese Han population with psoriasis vulgaris and generalized pustular psoriasis.

Project description: Not available

| S-EPMC4227539 | biostudies-literature

Upregulation of BTN3A1 on CD14+ cells promotes Vγ9Vδ2 T cells activation in psoriasis vulgaris

Project description:Vγ9Vδ2 T cells play an important role in the development and progression of psoriasis vulgaris (PV), but how they promote skin inflammation and the molecular mechanisms underlying Vγ9Vδ2 T cell dysfunction are poorly understood. Here, we show that circulating Vγ9Vδ2 T cells are decreased and exhibit enhanced proliferation and increased production of IFN-γ and TNF-α in PV patients. Monocytes from PV patients express higher levels of the phosphoantigen sensor butyrophilin 3A1 (BTN3A1) than monocytes from healthy controls. Blockade of BTN3A1 suppresses Vγ9Vδ2 T cell activation and abolishes the difference in Vγ9Vδ2 T cell activation between PV patients and healthy controls. The CD14+ cells in PV skin lesions highly express BTN3A1 and juxtapose to Vδ2 T cells. In addition, IFN-γ induces the up-regulation of BTN3A1 on monocytes. Collectively, our results demonstrate a crucial role of BTN3A1 on monocytes in regulating Vγ9Vδ2 T cell activation and highlight BTN3A1 as a potential therapeutic target for psoriasis.

2022-11-09 | GSE173387 | GEO

"Autoinflammatory psoriasis"-genetics and biology of pustular psoriasis.

Project description:Psoriasis is a chronic inflammatory skin condition that has a fairly wide range of clinical presentations. Plaque psoriasis, which is the most common manifestation of psoriasis, is located on one end of the spectrum, dominated by adaptive immune responses, whereas the rarer pustular psoriasis lies on the opposite end, dominated by innate and autoinflammatory immune responses. In recent years, genetic studies have identified six genetic variants that predispose to pustular psoriasis, and these have highlighted the role of IL-36 cytokines as central to pustular psoriasis pathogenesis. In this review, we discuss the presentation and clinical subtypes of pustular psoriasis, contribution of genetic predisposing variants, critical role of the IL-36 family of cytokines in disease pathophysiology, and treatment perspectives for pustular psoriasis. We further outline the application of appropriate mouse models for the study of pustular psoriasis and address the outstanding questions and issues related to our understanding of the mechanisms involved in pustular psoriasis.

| S-EPMC8027616 | biostudies-literature

Pathophysiology of Generalized Pustular Psoriasis.

Project description:Generalized pustular psoriasis (GPP) is a rare, severe form of pustular psoriasis characterized by widespread, recurrent episodes of neutrophil-rich pustule formation in the epidermis, which can be accompanied by fever and systemic inflammation. Recent clinical, histologic, and genetic evidence indicates that GPP is a distinct entity from plaque psoriasis, with different cytokine pathways predominant in the manifestation of each disease. The interleukin-36 (IL-36) signaling cascade plays a key role in regulating the innate immune system, and its dysregulation appears central to the pathogenesis of GPP. The altered expression of various IL-36 pathway constituents has been shown to cause a positive feedback loop of uncontrolled signaling and excess production of inflammatory cytokines, which in turn leads to chemokine induction and neutrophil recruitment in the epidermis. Given the potentially life-threatening nature of GPP episodes, drug interventions that rapidly achieve disease resolution are required. Early phase data indicate that treatments targeting various components of the IL-36 inflammatory cascade represent promising areas of research. However, there are currently no therapeutic agents specifically approved for GPP in the USA or Europe. Understanding the inflammatory pathways, associated risk factors, and role of neutrophils in the manifestation and perpetuation of GPP flares remains a key goal in developing effective therapeutics. In this article, we summarize the current understanding of GPP, describe novel therapeutic opportunities, and detail how the unique pathophysiology of the disease may inform future treatment strategies.

| S-EPMC8801405 | biostudies-literature

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