Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

MicroRNAs in Nasal Lavage Extracellular Vesicles as Potential Therapeutic Targets for Mucus Hypersecretion

ABSTRACT: MicroRNAs in Nasal Lavage Extracellular Vesicles as Potential Therapeutic Targets for Mucus Hypersecretion

PROVIDER: PRJNA1046545 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR26990618.fastq.gz	Fastqsanger.gz
	SRR26990619.fastq.gz	Fastqsanger.gz
	SRR26990620.fastq.gz	Fastqsanger.gz
	SRR26990621.fastq.gz	Fastqsanger.gz
	SRR26990622.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 18

Similar Datasets

MicroRNAs in Nasal Lavage Extracellular Vesicles as Potential Therapeutic Targets for Mucus Hypersecretion

Project description:Small RNA sequencing was conducted to identify the miRNAs responsible for AR using exosomes isolated from the nasal lavage (NAL) fluid of the control (n=9) and AR patient groups (n=8).

2023-12-04 | GSE248991 | GEO

Proteomics and metabolomics analysis of nasal lavage fluid in chronic rhinosinusitis with nasal polyps

Project description:Induced sputum cells (ISCs) and nasal lavage fluid cells (NLFCs) from 6 patients with CRSwNP, 6 patients suffering from CRSwNP with asthma, and 6 control subjects were procured in the study.

2023-02-20 | PXD040299 |

Label free Quantitative Proteomics analysis of Nasal lavage fluid rhinosinusitis

Project description:The study aimed to identify proteins associated with chronic rhinosinusitis with nasal polyps. Samples from nasal Lavage fluid from CRSwNP patients and controls were analysed and revealed a significant difference in protein expression. Dysregulated proteins were linked to airway inflammation, immune response and oxidative stress.

2024-10-22 | MSV000096171 | MassIVE

Proteomic analysis of mucus from chronic rhinosinusitis patients with or without nasal polyps

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

Application of text mining to build AOP-based mucus hypersecretion genesets and validation with in vitro and clinical samples

Project description:Purpose: Build genesets using text mining and validate the geneset with data from public repository and a dataset generated in house using in vitro models and RNA-seq Methods: Mucus hypersecretion and mucociliary dysfucntion adverse outcome pathways (AOPs) genesets were build using the text mining method described by Rani et al., 2015. Validation was performed using RNA expression data from cigarette and e-cigarette aerosol treated cells, IL-13 treated airway cells, and COPD-lung biopsies. The cigarette and e-cigarette aerosol RNA-samples from airway cells were generated and sequenced in house. The other dataset were publically available. Results: Using unsupervised clustering, the mucus hypersecretion and mucociliary dysfunction genesets were able to discriminate the cigartte treated cells from the e-cigarettes and the air control. The e-cigarette and the air control clustered together. Clustering was also observed with IL-13 treated cells. IL-13 is an induced of mucus hypersecretion. Clustering was not observed when COPD RNA-seq samples were used. PCA analysis revealed some degree of grouping based on disease status, but this was also heavily confounded by other parameters. Conclusions: Our study described the first application of text mining to build genesets relevant to AOPs. In vitro validation confirmed the genesets could discriminates between treatment that induce mucus hypersecretion phenotypes, however this could not be confirmed with COPD biopsy samples. This could be due to a series of technical confouding factors and the heterogeneity of the COPD disease.

2020-04-30 | GSE142100 | GEO

Proteomic analysis of mucus from chronic rhinosinusitis patients with or without nasal polyps

2016-07-22 | MSV000079984 | MassIVE

Pasteurella multocida from deep nasal swabs and tracheobronchial lavage in calves

Project description:Pasteurella multocida from deep nasal swabs and tracheobronchial lavage in calves

| PRJEB73847 | ENA

COPD lungs show an attached stratified mucus layer resembling the protective colonic mucus

Project description:Mucus accumulation is a key feature of respiratory diseases such as cystic fibrosis (CF) and chronic obstructive pulmonary disease (COPD). This is associated with goblet cell metaplasia and mucin overexpression, which can be induced by the increased activity of neutrophil elastase. The aim of the study was to characterization of mucus and epithelial cell proteomics in a porcine pancreatic elastase (PPE) mouse model of COPD/CF. The major proteins detected in mucus plugs obtained from PPE-treated mice included mucins Muc5ac and Muc5b, mucus-related proteins Clca1, Fcgbp, and Bpifb1. These proteins were upregulated in bronchoalveolar lavage (BAL) fluid and epithelial cells in mice exposed to elastase. Similar changes were found in BAL fluid of COPD patients.

2018-10-22 | PXD006770 | Pride

Phosphoproteome of SARS-CoV-2 infected Human Nasal Epithelium

Project description:The nasal epithelium is the primary initial site of SARS-CoV-2 entry in the human body. Since much of the molecular detail defining coronavirus entry and replication was derived from non-nasal cell lines, it remains unclear how SARS-CoV-2 overcomes the physical nasal mucus and periciliary mucin layers to infect and spread through the nasal epithelium. Using air-liquid interface cultured primary nasal epithelial cells, we observed that SARS-CoV-2 attaches to motile cilia during the initial stage of infection. Depletion of cilia inhibited SARS-CoV-2, as well as respiratory syncytial virus and parainfluenza virus infection, suggesting a widely-used ciliary mechanism for respiratory viral entry. Using electron and immunofluorescence microscopy, we further observed that SARS-CoV-2 progeny virions attached to airway microvilli 24 hours post infection and triggered the formation of apically extended and highly branched microvilli that organize viral egress from the microvillar base back into the mucus layer, supporting a model of virus dispersion throughout airway tissue via mucociliary transport. Chemical perturbation of microvillus formation severely impaired viral egress and subsequent spread. Phosphoproteomic analyses indicate that virally-triggered microvillar branching is linked to the p21-activated kinase 1 and 4 (PAK1/4) signaling pathway and viral infection is impaired by PAK1/4 kinase inhibitors. Our work provides insight into the mechanisms by which SARS-CoV-2 and potentially many respiratory viruses penetrate the physical nasal epithelium barrier, a first line of defense against pathogens, thus revealing a new view of the motile cilia and microvilli as critical host factors required for viral entry and egress.

2023-03-10 | PXD028123 | Pride

A common polymorphism in the Intelectin-1 gene influences mucus plugging in severe asthma

Project description:By incompletely understood mechanisms, type 2 (T2) inflammation present in the airways of severe asthmatics drives the formation of pathologic mucus which leads to airway mucus plugging. Here we investigate the molecular role and clinical significance of intelectin-1 (ITLN-1) in the development of pathologic airway mucus in asthma. Through analyses of human airway epithelial cells we find that ITLN1 gene expression is highly induced by interleukin-13 (IL-13) in a subset of metaplastic MUC5AC+ mucus secretory cells, and that ITLN-1 protein is a secreted component of IL-13-induced mucus. Additionally, we find ITLN-1 protein binds the C-terminus of the MUC5AC mucin and that its deletion in airway epithelial cells partially reverses IL-13-induced mucostasis. Through analysis of nasal airway epithelial brushings, we find that ITLN1 is highly expressed in T2-high asthmatics, when compared to T2-low children. Furthermore, we demonstrate that ITLN1 gene expression is significantly reduced and ITLN-1 protein expression is lost through a common genetic variant that is associated with protection from the formation of mucus plugs in T2-high asthma. This work identifies one of the first biomarkers and targetable pathways for the treatment of mucus obstruction in asthma.

2024-04-04 | GSE254127 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data