Gene Expression Profiles in Chronic Idiopathic Urticaria
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE57178 | GEO | 2014/08/12
SECONDARY ACCESSION(S): PRJNA245834
REPOSITORIES: GEO
Similar Datasets
Project description:Lesions of chronic idiopathic urticaria (CIU) showed significant up-regulation of 506 genes and reduced expression of 51 genes. Those most up-regulated are predominantly involved in cell adhesion (e.g. SELE), cell activation (e.g. CD69), and chemotaxis (e.g. CCL2). Twelve independent canonical pathways with p ≤ 0.001 were identified (including intracellular kinase pathways (RAN and JAK/Interferon), cytokine signaling pathways (IL-9, IL10, and IFN), a strong inflammatory response (interferon, IL-9, IL-10, iNOS, and glucocorticoid pathways) and increased cell proliferation (RAN signaling, cell cycle control, and tRNA charging). In addition, cellular functions associated with viral infections were dramatically up-regulated (activation z-score= 5.1; p = 4.97 X 10^-10). We enrolled 8 patients with CIU and 6 healthy controls and obtained 4mm punch biopsies of active lesions and unaffected skin of patients with CIU and of skin from normal controls. Routine histologic evaluation was performed, RNA was isolated and gene expression data was determined using an Affymetrix Human Gene 1.0 ST Array (www.affymetrix.com). Due to technical reasons, the final evaluation included 6 samples of lesional skin, 7 samples of non-lesional skin and 5 samples of normal skin.
2014-08-12 | E-GEOD-57178 | biostudies-arrayexpress
Project description:Chronic spontaneous urticaria (CSU), also traditionally called Chronic Idiopathic Urticaria (CIU), is a common dermatosis. Its estimated point prevalence is 0.6 to 1%. CSU is defined by spontaneously occurring short-lived and itching wheal, angioedema or both. The current nomenclature of urticaria endorses the use of a clinical rather than an aetiological classification to recognise that a percentage of patients with CSU have an autoimmune rather than idiopathic aetiology. As it happens with other IgE-associated diseases, a better knowledge of urticaria patients requires defining phenotypes. The present knowledge about CSU phenotypes is based on the clinical characteristics, associated comorbidities, the course of the disease and its response to the available effective drugs. But a phenotype is defined as the visible characteristics or traits that are a consequence of the expression of genes as well as the influence of environmental factors. The phenotype is part a consequence of the genotype. To study which is the genotype expressed by the patients suffering of CSU can be interesting. The mechanisms involved in the mast cell activation and the role of the released mast cell mediators are well known allowing explaining of how the wheals appear and disappear. But very little is known about the genetic susceptibility and genes involved in the development of wheals in CSU patients. By means of this work, enough case series was collected to draw reliable conclusions, based on the genetic variations found. In order to assess associations between genetic polymorphisms and the different phenotypes of CSU, large case series of well-documented patients with a relevant history are needed. The primary purpose of this study was to identify the most relevant genes expressed in the tissue and the blood samples from patients with moderate and severe CSU.
2017-04-19 | GSE72541 | GEO
Project description:Chronic spontaneous urticaria (CSU), also traditionally called Chronic Idiopathic Urticaria (CIU), is a common dermatosis. Its estimated point prevalence is 0.6 to 1%. CSU is defined by spontaneously occurring short-lived and itching wheal, angioedema or both. The current nomenclature of urticaria endorses the use of a clinical rather than an aetiological classification to recognise that a percentage of patients with CSU have an autoimmune rather than idiopathic aetiology. As it happens with other IgE-associated diseases, a better knowledge of urticaria patients requires defining phenotypes. The present knowledge about CSU phenotypes is based on the clinical characteristics, associated comorbidities, the course of the disease and its response to the available effective drugs. But a phenotype is defined as the visible characteristics or traits that are a consequence of the expression of genes as well as the influence of environmental factors. The phenotype is part a consequence of the genotype. To study which is the genotype expressed by the patients suffering of CSU can be interesting. The mechanisms involved in the mast cell activation and the role of the released mast cell mediators are well known allowing explaining of how the wheals appear and disappear. But very little is known about the genetic susceptibility and genes involved in the development of wheals in CSU patients. By means of this work, enough case series was collected to draw reliable conclusions, based on the genetic variations found. In order to assess associations between genetic polymorphisms and the different phenotypes of CSU, large case series of well-documented patients with a relevant history are needed. The primary purpose of this study was to identify the most relevant genes expressed in the tissue and the blood samples from patients with moderate and severe CSU.
2017-04-19 | GSE72540 | GEO
Project description:To determine whether lncRNAs are involved in chronic spontaneous urticaria (CSU), we analyzed the expression profile of lncRNAs and mRNAs in CSU.
2022-01-26 | GSE185516 | GEO
Project description:Chronic spontaneous urticaria (CSU), also traditionally called Chronic Idiopathic Urticaria (CIU), is a common dermatosis. Its estimated point prevalence is 0.6 to 1%. CSU is defined by spontaneously occurring short-lived and itching wheal, angioedema or both. The current nomenclature of urticaria endorses the use of a clinical rather than an aetiological classification to recognise that a percentage of patients with CSU have an autoimmune rather than idiopathic aetiology. As it happens with other IgE-associated diseases, a better knowledge of urticaria patients requires defining phenotypes. The present knowledge about CSU phenotypes is based on the clinical characteristics, associated comorbidities, the course of the disease and its response to the available effective drugs. But a phenotype is defined as the visible characteristics or traits that are a consequence of the expression of genes as well as the influence of environmental factors. The phenotype is part a consequence of the genotype. To study which is the genotype expressed by the patients suffering of CSU can be interesting. The mechanisms involved in the mast cell activation and the role of the released mast cell mediators are well known allowing explaining of how the wheals appear and disappear. But very little is known about the genetic susceptibility and genes involved in the development of wheals in CSU patients. By means of this work, enough case series was collected to draw reliable conclusions, based on the genetic variations found. In order to assess associations between genetic polymorphisms and the different phenotypes of CSU, large case series of well-documented patients with a relevant history are needed. The primary purpose of this study was to identify the most relevant genes expressed in the tissue and the blood samples from patients with moderate and severe CSU. Objective: The primary purpose of this study was to identify the most relevant genes expressed in the tissue and the blood samples from patients with moderate and severe CSU. The knowledge of the gene profiling differences comparing wheal versus no-lesion skin in selected patients is a real and accurate approach to identify the genes expressed in the wheal developed in patients with CSU. Patients and methods: A total of 20 patients suffering of moderate and severe CSU/CIU and 10 healthy control subjects were included. The setting of the study was the Department of Dermatology and the Department of Pharmacology Clinic at the Hospital del Mar, Institut Mar d'Investigacions Mediques, Barcelona. The sample size is adequate to the exploratory character of the study. Only patients showing active moderate to severe CSU during at least 3 months were included in the study. Patients were selected prospectively. An Urticaria Activity Score (UAS) 7 defined moderate to severe CSU, this mean an UAS7 �16 (UAS 7 range from 0 to 42), where the symptom itch showed a value �8. All the patients included remained symptomatic in spite of the treatment with antihistamines. The diagnosis of CSU was based on clinical history data and physical examination. Any active treatment was supplied at the patient at the time where the samples were obtained. Healthy controls were selected from a pool of volunteers. A detailed anamnesis, clinical exploration and basal blood analysis was carried out in order to guarantee that any active disease nor cutaneous nor systemic was present. The CSU patients and the healthy volunteers were submitted to some interventions in order to obtain cutaneous and venous blood samples. Cutaneous biopsies were obtained after local anesthesia using punch biopsy of 4 mm in diameter. Two cutaneous biopsies including skin from an active wheal and one biopsy from non-lesion skin were obtained. The active wheal chosen for biopsy was obtained from the trunk and clinically showed erythema and edema, with a time of evolution of at least of one hour. One of the biopsies taken from the wheal was fixed in formaldehyde and after paraffin inclusion was stained with haematoxilin -eosin, Giemsa and with c-Kit as mast cell marker with the objective to characterize the diagnosis of wheal and describe accurately the characteristics of the inflammatory infiltrate. The second biopsy was immediately prepared for storage prior to be submitted for gene array. Fat and other undesired components that do not belong to the sample were removed before quick-freezing the tissue in liquid nitrogen. Cryopreserved tissue samples were stored at -80°C prior to the gene microarray study. The punch taken over no-lesion skin guarantee that no wheal was present in the previous 72 hours and no other skin alteration was present i.e., desquamation or pigmentation. Venous blood analysis was obtained from the basilic mediana vein in the antecubital fossae and prepared for its storage for gene array analysis. Quality control of RNA samples was performed with the Bioanalyzer 2100 (Agilent Technologies, Palo Alto, CA, USA). Good quality samples with an RNA Integrity Number (RIN) value >6, and also some mildly degraded samples with a RIN value between 4 and 6, were processed following specific protocols. The hybridization procedure was performed according to the Agilent 60-mer oligo microarray processing protocol using the Agilent Gene Expression Hybridization Kit (Agilent Technologies). Based on the results provided from the microarray comparative analysis, we selected a set of genes to be confirmed by Q-PCR. The criteria followed to perform such selection were based in technical aspects that would guarantee gene confirmation. These recommendations include an adjusted P value of 0.05 and a Log fold change of 1 (plus or minor to 1). The second criteria was based in an accurate analysis of the genes up or down regulated and its possible involvement in mast cell biology, wheal pathogenesis, urticaria or allergy. The data base included shows the raw data of the gene-array performed in the available samples of the blood and the tissue of the patients with CSU and the healthy controls included in this study. 61 samples were analyzed from 30 individuals, 20 patients and 10 healthy controls. This Series includes the samples from tissue.
2017-04-19 | E-GEOD-72540 | biostudies-arrayexpress
Project description:Chronic spontaneous urticaria (CSU), also traditionally called Chronic Idiopathic Urticaria (CIU), is a common dermatosis. Its estimated point prevalence is 0.6 to 1%. CSU is defined by spontaneously occurring short-lived and itching wheal, angioedema or both. The current nomenclature of urticaria endorses the use of a clinical rather than an aetiological classification to recognise that a percentage of patients with CSU have an autoimmune rather than idiopathic aetiology. As it happens with other IgE-associated diseases, a better knowledge of urticaria patients requires defining phenotypes. The present knowledge about CSU phenotypes is based on the clinical characteristics, associated comorbidities, the course of the disease and its response to the available effective drugs. But a phenotype is defined as the visible characteristics or traits that are a consequence of the expression of genes as well as the influence of environmental factors. The phenotype is part a consequence of the genotype. To study which is the genotype expressed by the patients suffering of CSU can be interesting. The mechanisms involved in the mast cell activation and the role of the released mast cell mediators are well known allowing explaining of how the wheals appear and disappear. But very little is known about the genetic susceptibility and genes involved in the development of wheals in CSU patients. By means of this work, enough case series was collected to draw reliable conclusions, based on the genetic variations found. In order to assess associations between genetic polymorphisms and the different phenotypes of CSU, large case series of well-documented patients with a relevant history are needed. The primary purpose of this study was to identify the most relevant genes expressed in the tissue and the blood samples from patients with moderate and severe CSU. Objective: The primary purpose of this study was to identify the most relevant genes expressed in the tissue and the blood samples from patients with moderate and severe CSU. The knowledge of the gene profiling differences comparing wheal versus no-lesion skin in selected patients is a real and accurate approach to identify the genes expressed in the wheal developed in patients with CSU. Patients and methods: A total of 20 patients suffering of moderate and severe CSU/CIU and 10 healthy control subjects were included. The setting of the study was the Department of Dermatology and the Department of Pharmacology Clinic at the Hospital del Mar, Institut Mar d'Investigacions Mediques, Barcelona. The sample size is adequate to the exploratory character of the study. Only patients showing active moderate to severe CSU during at least 3 months were included in the study. Patients were selected prospectively. An Urticaria Activity Score (UAS) 7 defined moderate to severe CSU, this mean an UAS7 �16 (UAS 7 range from 0 to 42), where the symptom itch showed a value �8. All the patients included remained symptomatic in spite of the treatment with antihistamines. The diagnosis of CSU was based on clinical history data and physical examination. Any active treatment was supplied at the patient at the time where the samples were obtained. Healthy controls were selected from a pool of volunteers. A detailed anamnesis, clinical exploration and basal blood analysis was carried out in order to guarantee that any active disease nor cutaneous nor systemic was present. The CSU patients and the healthy volunteers were submitted to some interventions in order to obtain cutaneous and venous blood samples. Cutaneous biopsies were obtained after local anesthesia using punch biopsy of 4 mm in diameter. Two cutaneous biopsies including skin from an active wheal and one biopsy from non-lesion skin were obtained. The active wheal chosen for biopsy was obtained from the trunk and clinically showed erythema and edema, with a time of evolution of at least of one hour. One of the biopsies taken from the wheal was fixed in formaldehyde and after paraffin inclusion was stained with haematoxilin -eosin, Giemsa and with c-Kit as mast cell marker with the objective to characterize the diagnosis of wheal and describe accurately the characteristics of the inflammatory infiltrate. The second biopsy was immediately prepared for storage prior to be submitted for gene array. Fat and other undesired components that do not belong to the sample were removed before quick-freezing the tissue in liquid nitrogen. Cryopreserved tissue samples were stored at -80°C prior to the gene microarray study. The punch taken over no-lesion skin guarantee that no wheal was present in the previous 72 hours and no other skin alteration was present i.e., desquamation or pigmentation. Venous blood analysis was obtained from the basilic mediana vein in the antecubital fossae and prepared for its storage for gene array analysis. Quality control of RNA samples was performed with the Bioanalyzer 2100 (Agilent Technologies, Palo Alto, CA, USA). Good quality samples with an RNA Integrity Number (RIN) value >6, and also some mildly degraded samples with a RIN value between 4 and 6, were processed following specific protocols. The hybridization procedure was performed according to the Agilent 60-mer oligo microarray processing protocol using the Agilent Gene Expression Hybridization Kit (Agilent Technologies). Based on the results provided from the microarray comparative analysis, we selected a set of genes to be confirmed by Q-PCR. The criteria followed to perform such selection were based in technical aspects that would guarantee gene confirmation. These recommendations include an adjusted P value of 0.05 and a Log fold change of 1 (plus or minor to 1). The second criteria was based in an accurate analysis of the genes up or down regulated and its possible involvement in mast cell biology, wheal pathogenesis, urticaria or allergy. The data base included shows the raw data of the gene-array performed in the available samples of the blood and the tissue of the patients with CSU and the healthy controls included in this study. 61 samples were analyzed from 30 individuals, 20 patients and 10 healthy controls. This Series includes the samples from blood.
2017-04-19 | E-GEOD-72541 | biostudies-arrayexpress
Project description:Gene Expression Profiles in Chronic Idiopathic Urticaria
| PRJNA245834 | ENA
Project description: Not available
| S-EPMC3432140 | biostudies-literature
Project description:Gene expression profile of patients with moderate and severe chronic spontaneous urticaria
| PRJNA294297 | ENA
Project description:New onsets of chronic urticaria (CU) have been reported after repeated immunizations, mainly with the Moderna mRNA-1273 vaccine (Spikevax). This study aims to evaluate patients with CU after COVID-19 mRNA vaccination. The contribution of SARS-Cov2 infection, atopy and IgE against the vaccine was analyzed. We monitored the features of patients who developed CU after vaccination in the Canton of Vaud through two surveys conducted in 2022 and 2023. Fifty individuals with CU underwent blood tests, and their results were compared with individuals without a history of urticaria (N=135). The presence of anti-vaccine IgE was detected with basophil activation tests (BAT). We assessed anti-SARS-Cov2 humoral response, and the presence of IgEs against common respiratory allergens (Phadiatop) as a surrogate for atopy. Post-vaccination CU occurred after a median interval of 10 days and significantly more after the Spikevax booster, affecting middle-aged individuals (median 41, 66% females). In 2023, CU was still active in 53% of the cases. Inducible forms of CU, primarily dermographism, were reported in 54% (2022) and 61% (2023) of the cases. BAT positivity was not specific to CU, anti-nucleocapsid positivity, or atopy but was significantly associated with higher anti-spike neutralizing activities and younger age. Four CU patients tolerated an additional dose of mRNA vaccine with no disease exacerbation/recurrence. The spikevax booster induced anti-vaccine IgE independently of CU, the latter being not directly associated with COVID-19 infection nor atopy. The tolerance to a new booster in 4/4 patients suggests that the Spikevax vaccine indirectly triggered CU in predisposed individuals.
2024-07-26 | GSE272645 | GEO