Neutrophilic inflammation and epithelial barrier disruption in nasal polyps characterize NSAID-exacerbated respiratory disease
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ABSTRACT:
PROVIDER: PRJNA784182 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR17054628_1.fastq.gz | Fastqsanger.gz | |||
| SRR17054628_2.fastq.gz | Fastqsanger.gz | |||
| SRR17054629_1.fastq.gz | Fastqsanger.gz | |||
| SRR17054629_2.fastq.gz | Fastqsanger.gz | |||
| SRR17054630_1.fastq.gz | Fastqsanger.gz |
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Project description:Chronic rhinosinusitis with nasal polyps (CRSwNP) is a debilitating inflammatory disease of the sinonasal cavities. Concomitant CRSwNP and asthma, together with hypersensitivity reactions to cyclooxygenase-1 (COX-1) inhibitors, is a particular phenotype known as NSAID-exacerbated respiratory disease (N-ERD), which is associated with greater disease severity. In this study, we attempted to characterize clinical, laboratory, and transcriptomic differences between CRSwNP patients with N-ERD (N-ERD; N=13) and CRSwNP patients without N-ERD (non-N-ERD, N=13).
2021-12-15 | GSE189690 | GEO
Project description:NSAID-exacerbated respiratory disease (N-ERD) represents a particularly severe endotype of chronic rhinosinusitis with nasal polyps (CRSwNP), which affects around 10-16% of CRSwNP patients. N-ERD is characterized by severe and refractory nasal polyposis, bronchial asthma and intolerance to non-steroidal anti-inflammatory drugs (NSAIDs), including aspirin. Today, the pathogenesis of N-ERD remains incompletely understood and curative treatments are lacking. Using a global transcriptomic approach, we identified local changes between the mucosa of N-ERD nasal polyps and healthy control inferior turbinates. Nasal brushing samples were collected from inferior turbinates of healthy controls and nasal polyps of N-ERD patients under anterior rhinoscopy and stored at -80°C in RNAprotect until RNA isolation and RNAseq.
2020-06-30 | E-MTAB-7962 | biostudies-arrayexpress
Project description:Objective: We sought to obtain detailed information about transcriptional differences in epithelial cells and immune cell subsets present in polyps of aspirin-exacerbated respiratory disease and chronic rhinosinusitis with nasal polyps. Methods: After enrichment for various immune subsets by flow cytometric sorting of polyp-derived cells, we performed transcriptomic profiling by employing single-cell RNA sequencing of all patients. Results: Transcriptomic profiling revealed that epithelial and mast cells not only complement one another in terms of gene expression associated with the 15-lipoxygenase pathway, but also show a clear type 2 associated inflammatory phenotype as identified by the upregulation of POSTN, CCL26 and IL13 in patients with aspirin-exacerbated respiratory disease.
2022-04-20 | GSE196169 | GEO
Project description:The mechanisms underlying neutrophilic inflammation in chronic rhinosinusitis with nasal polyps (CRSwNP) remain poorly investigated. This study aimed to examine the factors that contribute to tissue neutrophilia in CRSwNP. The numbers of neutrophils and active caspase-3-positive apoptotic neutrophils in sinonasal tissues were assessed via immunofluorescence staining. The 95th percentile of tissue neutrophil numbers in control subjects was selected as a cut-off to define neutrophil-high (Neu-high) or neutrophil-low (Neu-low) nasal polyps (NPs). The levels of 34 inflammatory mediators in sinonasal tissues were analyzed using Bio-Plex assay. Purified human peripheral blood neutrophils were incubated with nasal tissue homogenates, and the apoptotic neutrophils were assessed via flow cytometry. The cut-off for Neu-high NPs was >10 myeloperoxidase positive cells/high-power field. Compared with Neu-low NPs, Neu-high NPs had higher tissue levels of IL-1β, IL-1Ra, IL-6, IL-8, G-CSF, MCP-1, and MIP-1α, but lower levels of IL-5, IL-13, IgE, and eosinophils. Principal component and multiple correspondence analyses revealed mixed type 1, type 2, and type 3 endotypes for Neu-low NPs, and predominant type 1 and type 3 endotypes for Neu-high NPs. Neu-high NPs had lower percentages of apoptotic neutrophils than Neu-low NPs. The numbers of neutrophils and the percentages of apoptotic neutrophils correlated with G-CSF and IL-6 levels in the NPs. Tissue homogenates from Neu-high NPs, but not those from Neu-low NPs, suppressed neutrophil apoptosis in vitro, which was reversed by anti-G-CSF treatment. Tissue neutrophil numbers were associated with difficult-to-treat disease in patients with CRSwNP after surgery. We propose that G-CSF promotes neutrophilic inflammation by inhibiting neutrophil apoptosis in CRSwNP.
| S-EPMC8718617 | biostudies-literature
Project description:Chronic rhinosinusitis with nasal polyps is a hallmaerk disease in the field of upper airway immunity and chronic inflammation. Diverse inflammatory patterns between nasal polyps have been described in patients that hail from disparate racial and geographic backgrounds. However, it remains unclear whether these immunologic differences in nasal polyps between racial groups are driven by unique molecular mechanisms. We interrogated the gene expression profiles of nasal polyp tissues from Western (United States) and East Asian (Japan) descent, compared to ethmoid sinus tissue controls.
2021-12-15 | GSE179268 | GEO
Project description:Chronic rhinosinusitis with nasal polyps is a hallmaerk disease in the field of upper airway immunity and chronic inflammation. Diverse inflammatory patterns between nasal polyps have been described in patients that hail from disparate racial and geographic backgrounds. However, it remains unclear whether these immunologic differences in nasal polyps between racial groups are driven by unique molecular mechanisms. We interrogated the gene expression profiles of nasal polyp tissues from Western (United States) and East Asian (Japan) descent, compared to ethmoid sinus tissue controls.
2021-12-15 | GSE179265 | GEO
Project description:Asthmatic chronic rhinosinusitis with nasal polyps (aCRSwNP) is a common disruptive eosinophilic disease. Therefore, we sought to identify gene expression changes in nasosinus inflamed mucosa and adjacent polyp tissue from subjects with aCRSwNP. Twelve asthmatic chronic rhinosinusitis (aCRS) subjects (11 with nasal polyps; aCRSwNP) provided inflamed nasosinus mucosa (11 samples) and adjacent polyp (10 samples) or a small mixed mucosa and polyp specimen (1 sample) (thus, 22 samples overall). Inflamed mucosa or polyp was from the middle meatus or anterior ethmoid cavity. As control samples, nasosinus tissue was collected from the inferior turbinate or uncinate process from normal or rhinitis subjects without nasal polyps (n=17); 4 had physician-diagnosed allergic rhinitis (AR), 2 had suspected AR, 1 had suspected vasomotor rhinitis, and 10 had no signs of nasosinus disease, allergy, or atopy. All 4 AR subjects chose to donate tissue outside of their known allergy season(s).
2010-08-12 | E-GEOD-23552 | biostudies-arrayexpress
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:Asthmatic chronic rhinosinusitis with nasal polyps (aCRSwNP) is a common disruptive eosinophilic disease. Therefore, we sought to identify gene expression changes in nasosinus inflamed mucosa and adjacent polyp tissue from subjects with aCRSwNP.
2010-08-12 | GSE23552 | GEO
Project description:Background: Alternative polyadenylation (APA) is emerging as a widespread mechanism of gene regulation. The usage of APA sites allows a single gene to encode multiple mRNA transcripts with different 3'-untranslated region (3'UTR) lengths. Many disease processes reflect the importance of the regulation of APA site switching. The objective of this study was to explore the profiling of tandem APA sites in nasal polyps compared with nasal uncinate process mucosa. Methods: Sequencing of APA sites (SAPAS) based on second-generation sequencing technology was undertaken to investigate the use of tandem APA sites and identify gene expression patterns in samples from the nasal polyps and nasal uncinate process mucosa of two patients with chronic rhinosinusitis with nasal polyps. The findings of the SAPAS analysis were validated via quantitative reverse-transcription polymerase chain reaction (qRT-PCR). Results: First, the results showed a switching of 3'UTR lengths in nasal polyps compared with nasal uncinate process mucosa. From the two patients, 105 overlapping genes in the nasal polyps were switched to distal poly(A) sites, and 90 such genes were switched to proximal poly(A) sites. Several Gene Ontology terms were enriched in the list of genes with switched APA sites, including transcription regulation, cell cycle, apoptosis, and metabolism. Second, we detected genes that showed differential expression with at least a 3-fold difference between nasal polyp tissue and nasal uncinate process mucosa. Between the two sample types, 627 genes exhibited differential expression. The qRT-PCR results confirmed our SAPAS results. Conclusion: APA site-switching events of 3'UTRs are prevalent in nasal polyp tissue, and the regulation of gene expression mediated by APA may play an important role in the formation and persistence of nasal polyps. Our results may provide new insights into the possible pathophysiologic processes involved in nasal polyps.
2012-12-31 | GSE39957 | GEO