Microarray analysis of epithelial and fibroblast cells in chronic rhinosinusitis
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE69093 | GEO | 2015/12/31
SECONDARY ACCESSION(S): PRJNA284516
REPOSITORIES: GEO
Similar Datasets
Project description:Chronic rhinosinusitis without polyps (CRSsNP) is typified by inflammation of the sinonasal epithelium and the development of fibrosis. The precise pathophysiology of this common condition remains elusive. Here we aim to investigate the transcriptome (RNA transcripts in the cell) of the component nasal epithelial and fibroblast cells in CRSsNP and health to identify if there are clusters of differentially expressed genes as possible novel CRS therapeutic targets. Gene expression profiling by Illumina BeadArray of primary nasal epithelial and fibroblast cells in heatlh and chronic sinusitis. Samples from consenting human donors (Epithelial Case, n=13, Epithelial Control, n=11, Fibroblast Case, n=12, Fibroblast Control, n=12).
2015-12-31 | E-GEOD-69093 | biostudies-arrayexpress
Project description:Chronic rhinosinusitis (CRS) is a heterogeneous disease characterized by local inflammation of the upper airways which persists for at least 12 weeks. CRS is one of the most common chronic diseases in adults in the United States, affecting over 30 million Americans. CRS is frequently divided into 2 types: CRS with nasal polyps (CRSwNP) and CRS without nasal polyps (CRSsNP). Histologic studies have demonstrated significant tissue eosinophilia in CRSwNP. T cells in the mucosa are elevated in both forms of CRS and are skewed towards Th2 cytokine expression in CRSwNP. However pathogenic role of CRS has not been fully explored. To screen for pathogenic factors in CRS, we performed a microarray study. We collected uncinate tissues (UT) from 6 subjects with CRSsNP, 6 subjects with CRSwNP and 6 control subjects and nasal polyp (NP) tissues from 6 subjects with CRSwNP and then evaluated gene expression profiles using Affymetrix Human Genome U133 plus 2.0 array. We collected UT from control subjects and pathients with CRSsNP and CRSwNP, and nasal polyp tissues from patients with CRSwNP. Gene expression profiles were evaluated using Human Genome U133 plus 2.0 array (Affymetrix).
2012-03-27 | E-GEOD-36830 | biostudies-arrayexpress
Project description:Chronic rhinosinusitis (CRS) is a heterogeneous disease characterized by local inflammation of the upper airways which persists for at least 12 weeks. CRS is one of the most common chronic diseases in adults in the United States, affecting over 30 million Americans. CRS is frequently divided into 2 types: CRS with nasal polyps (CRSwNP) and CRS without nasal polyps (CRSsNP). Histologic studies have demonstrated significant tissue eosinophilia in CRSwNP. T cells in the mucosa are elevated in both forms of CRS and are skewed towards Th2 cytokine expression in CRSwNP. However pathogenic role of CRS has not been fully explored. To screen for pathogenic factors in CRS, we performed a microarray study. We collected uncinate tissues (UT) from 6 subjects with CRSsNP, 6 subjects with CRSwNP and 6 control subjects and nasal polyp (NP) tissues from 6 subjects with CRSwNP and then evaluated gene expression profiles using Affymetrix Human Genome U133 plus 2.0 array.
2012-03-28 | GSE36830 | GEO
Project description:RNA sequencing (RNAseq) is being used to study inflammatory pathways in chronic rhinosinusitis (CRS). Our goal was to probe validity of tissue eosinophilia as a metric to study RNAseq in CRS. The study was conducted on prospectively enrolled subjects undergoing sinonasal surgery. Subjects were categorized as control, CRS, CRS with nasal polyps (CRSwNP) and CRS without nasal polyps (CRSsNP). CRS was also categorized by tissue eosinophil levels per high power field (EOS/HPF) as <10 EOS/HPF or ≥10 EOS/HPF. Ethmoidal tissue samples were processed, differentially expressed (DE) genes were calculated and Ingenuity pathway analysis (IPA) performed.Controls separated clearly from CRS by both study criteria (polyp status, EOS/HPF). In both analyses, CRS differentiated into two distinct CRS subgroups. However, heatmaps showed greater homogeneity within each CRS subtype when studied by eosinophilia versus polyp status. Overall, high differential gene expression was found in CRS versus controls, with 736 statistically significant differentially expressed (DE) genes. On comparison between between CRSwNP and CRSsNP, 60 DE genes were found and on analyzing by tissue EOS/HPF, 110DE genes were statistically significant between CRS <10 EOS/HPF and CRS ≥10 EOS/HPF analyses. Tissue eosinophilia as a metric was further validated by finding of IL 17 signalling pathway between <10EOS/HPF (increased) versus ≥10 EOS/HPF samples on pathway analysis. As a metric, tissue eosinophilia is at least as effective as analysis by polyp status for RNA sequencing and may potentially offer superior insights into mechanistic pathways.
2022-03-21 | GSE198950 | GEO
Project description:Patients with chronic rhinosinusitis (CRS) have abnormal immune responses triggered by a variety of infectious agents, airborne toxins and fungi. Respiratory epithelial cells serve as relay stations capable of amplifying or augmenting cues received from external stimuli to nearby immune cells located in the sinus mucosa. Previous studies have identified increases in complement components and complement gene expression in the mucosa of patients with atopic CRS with nasal polyps (CRSwNP). As part of a larger study, we used shotgun proteomics to quantify changes in mucus proteins between patients with and without nasal polyps.
2016-05-26 | PXD004144 | Pride
Project description:Primarily on the basis of the absence or presence of nasal polyps (NPs)Chronic Rhinosinusitis(CRS) is often classified as CRS with nasal polyps (CRSwNP) and CRS without nasal polyps (CRSsNP). CRSwNP remains a signifificant public health problem with a considerable socioeconomic burden. The previous research reported that the pathophysiology of CRSwNP is a complex multifactorial disease. There have been many studies on its etiology, but its pathogenesis remains unclear. Dysregulated expression of miRNAs has been shown in psoriasis, rheumatoid arthritis, pulmonary fibrosis, and allergic asthma. CircRNA is also involved in the inflammatory diseases, such as in rheumatoid arthritis, septic acute kidney injury, myocardial ischemia/reperfusion injury, epsis-induced liver damage and so on. Especially, the function of miRNA is research hotspots, including in CRSwNP. While, the study on circRNA in CRSwNP is still unknown. Additionally, according to the different percentage of eosinophil, CRSwNP was further divided into eosinophilic CRSwNP (ECRSwNP) and non-ECRSwNP. However, little is known about the functions of circRNAs and miRNAs in CRSwNP. The study is aimed to investigate the expression of circular RNA (circRNA) and microRNA (miRNAs) in CRSwNP and control group, to conform whether these molecules are related with the occurrence and development of CRSwNP. We aimed to compare the microarray expression profile of miRNAs and circRNAs in nasal polyps of CRSwNP and normal nasal mucosa from control subjects.
2021-03-23 | GSE169376 | GEO
Project description:Primarily on the basis of the absence or presence of nasal polyps (NPs)Chronic Rhinosinusitis(CRS) is often classified as CRS with nasal polyps (CRSwNP) and CRS without nasal polyps (CRSsNP). CRSwNP remains a signifificant public health problem with a considerable socioeconomic burden. The previous research reported that the pathophysiology of CRSwNP is a complex multifactorial disease. There have been many studies on its etiology, but its pathogenesis remains unclear. Dysregulated expression of miRNAs has been shown in psoriasis, rheumatoid arthritis, pulmonary fibrosis, and allergic asthma. CircRNA is also involved in the inflammatory diseases, such as in rheumatoid arthritis, septic acute kidney injury, myocardial ischemia/reperfusion injury, epsis-induced liver damage and so on. Especially, the function of miRNA is research hotspots, including in CRSwNP. While, the study on circRNA in CRSwNP is still unknown. Additionally, according to the different percentage of eosinophil, CRSwNP was further divided into eosinophilic CRSwNP (ECRSwNP) and non-ECRSwNP. However, little is known about the functions of circRNAs and miRNAs in CRSwNP. The study is aimed to investigate the expression of circular RNA (circRNA) and microRNA (miRNAs) in CRSwNP and control group, to conform whether these molecules are related with the occurrence and development of CRSwNP. We aimed to compare the microarray expression profile of miRNAs and circRNAs in nasal polyps of CRSwNP and normal nasal mucosa from control subjects.
2021-03-23 | GSE169375 | GEO
Project description:Patients with chronic rhinosinusitis (CRS) have abnormal immune responses triggered by a variety of infectious agents, airborne toxins and fungi. Respiratory epithelial cells serve as relay stations capable of amplifying or augmenting cues received from external stimuli to nearby immune cells located in the sinus mucosa. Previous studies have identified increases in complement components and complement gene expression in the mucosa of patients with atopic CRS with nasal polyps (CRSwNP). As part of a larger study, we used shotgun proteomics to quantify changes in mucus proteins between patients with and without nasal polyps.
2016-07-22 | MSV000079984 | MassIVE
Project description:Considering the complex and multifarious features of Chronic rhinosinusitis (CRS) including immunologic patterns, novel modalities are needed to reflect clinical and pathophysiological endotypes beyond nasal polyps.We aimed to investigate the proteome of nasal secretions on filter paper from CRS patients to characterize endotypes.
2019-07-29 | PXD013330 | Pride
Project description:Chronic rhinosinusitis is classified into eosinophilic chronic rhinosinusitis (ECRS) and non-eosinophilic chronic rhinosinusitis (NECRS). ECRS is a refractory allergic disease involving a variety of immune and epithelial cells. S100A8 is a damage-associated molecular pattern that is closely related to allergic inflammation. However, the pathological implications of S100A8 in ECRS have not been clarified. We evaluated the role of S100A8 in the pathogenesis of ECRS. Gene expression profiles of nasal polyps obtained from patients with ECRS or NECRS were evaluated using RNA sequencing. S100A8 was identified as a significantly upregulated gene in nasal polyps associated with ECRS. Consistently, immunohistochemistry revealed that S100A8 stained intensely in nasal polyps from patients with ECRS. Human nasal epithelial cells expressed the receptor for advanced glycation end products and Toll-like receptor 4. Recombinant S100A8 protein induced interleukin-1β secretion in human nasal epithelial cells. Our data demonstrate that S100A8 induces production of interleukin-1β in the nasal epithelium, which may be involved in the pathogenesis of ECRS.
2022-09-11 | GSE172305 | GEO