Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

6ffd3567-257c-4747-90f9-e7e6f8241af2 - samples

ABSTRACT: Single cell RNA sequence generated from human primary nasal epithelium differentiated at air-liquid interface. This dataset comprises tissue from two donors, with cultures either unexposed or exposed to SARS-CoV2. Libraries were prepared using the 10X Genomics pipeline as per manufacturer's instructions.

PROVIDER: EGAD00001008159 | EGA |

REPOSITORIES: EGA

ACCESS DATA

Json Xml

Similar Datasets

scRNAseq of human primary nasal epithelium differentiated at air-liquid interface exposed to SARS-CoV2

Project description:The nasal epithelium is a plausible entry point for SARS-CoV-2, a site of pathogenesis and transmission, and may initiate the host response to SARS-CoV-2. Antiviral interferon responses are critical to outcome of SARS-CoV-2. Yet little is known about the interaction between SARS-CoV-2 and innate immunity in this tissue. Here we applied single-cell RNA sequencing and proteomics to a primary cell model of human primary nasal epithelium differentiated at air-liquid interface.

| EGAS00001005633 | EGA

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

Interferon signaling in the nasal epithelium distinguishes among lethal and common cold respiratory viruses and is critical for viral clearance

Project description:All respiratory viruses establish primary infections in the nasal epithelium, where efficient innate immune induction may prevent dissemination to the lower airway and thus minimize pathogenesis. Human coronaviruses (HCoVs) cause a range of pathologies, but the host and viral determinants of disease during common cold versus lethal HCoV infections are poorly understood. We model the initial site of infection using primary nasal epithelial cells cultured at air-liquid interface (ALI). HCoV-229E, HCoV-NL63 and human rhinovirus-16 are common cold-associated viruses that exhibit unique features in this model: early induction of antiviral interferon (IFN) signaling, IFN-mediated viral clearance, and preferential replication at nasal airway temperature (33ºC) which confers muted host IFN responses. In contrast, lethal SARS-CoV-2 and MERS-CoV encode antagonist proteins that prevent IFN-mediated clearance in nasal cultures. Our study identifies features shared among common cold-associated viruses, highlighting nasal innate immune responses as predictive of infection outcomes and nasally-directed IFNs as potential therapeutics.

2024-03-25 | GSE253542 | GEO

Network Analysis Reveals Age- and Virus-Specific Circuits in Nasal Epithelial Cells of Extremely Premature Infants

Project description:Analysis of influenza A and respiratory synctial virus infections in cultured nasal epithelial cells at the air-liquid interface (ALI) of adult, term, and preterm infants.

2024-06-21 | GSE239726 | GEO

Strong correlation between air-liquid interface cultures and in vivo transcriptomics of nasal brush biopsy

Project description:Air-liquid interface cultures are extensively used to model chronic respiratory diseases. Comparative transcriptomics between cultured cells and fresh nasal brushings from patients suggests a high degree of correlation.

2020-07-31 | GSE145096 | GEO

Genome-wide gene expression analysis of upper airway (i.e., nasal) epithelial cells (i.e., RPMI 2650) exposed to fresh welding fumes

Project description:Inhaled welding fumes are deposited on all parts of the respiratory system, with the nasal cavity being the initial point of contact. We investigated the influence of fresh welding fumes on nasal epithelial model, i.e., RPMI 2650 cells, at the transcriptome level. Spark-generated welding fumes at two different concentrations (85 µg/m3 - low; 760 µg/m3 - high) were exposed to RPMI 2650 cell monolayers at air-liquid-interface continuously for 6h, followed by zero hours (or) four hours post-exposure incubation.

2014-12-01 | GSE62384 | GEO

Exploring intrinsic variability between cultured nasal and bronchial epithelia in cystic fibrosis

Project description:The nasal and bronchial epithelium are unified parts of the respiratory tract that are affected in the monogenic disorder cystic fibrosis (CF). Recent studies have uncovered that nasal and bronchial tissues exhibit intrinsic variability, including differences in mucociliary cell composition and expression of unique transcriptional regulatory proteins which relate to germ layer origin. In the present study, we explored transcriptomic differences between cultured nasal and bronchial epithelial cells from people with CF. Comparison of air-liquid interface-differentiated epithelial cells from subjects with CF revealed distinct mucociliary differentiation states of nasal and bronchial cultures. Moreover, using RNA sequencing we identified cell type-specific signature transcription factors in differentiated nasal and bronchial epithelial cells.

2023-11-21 | GSE241801 | GEO

Human Organotypic Smoke Street

Project description:The aim of this study was to develop human bronchial and nasal epithelium culture models that are relevant to investigate the impact of cigarette smoke (CS) observed in vivo in respiratory tract tissues in contact with inhaled CS. We used two organotypic cultures generated from primary cells derived from non-smoking donors that contain fibroblasts and epithelial cells in order to reproduce as closely as possible the in vivo situation. To mimic the smoking behavior of a moderate smoker during one day, human tissue cultures (bronchial and nasal epithelium) were exposed repeatedly and directly at the air/liquid interface (using the Vitrocell(R) System) to two doses (high 4.2 ug TPM/cm2 and low 2.2 ug TPM/cm2 per cigarette) of the whole smoke generated by one cigarette or to humidified air (sham). CS exposure was repeated four times with one hour intervals between each cigarette. Various endpoints (e.g., gene and microRNA expression, CYP activity, pro-inflammatory markers release, differential cell counts, cytotoxicity measurement) were then captured to assess the baseline (time 0) and early responses of the tissues after exposure (4 hours) as well as the recovery phase (24 and 48 hours).

2013-12-11 | E-MTAB-1721 | biostudies-arrayexpress

Expression data from regenerating human airway epithelium in vitro.

Project description:To identify transcriptomic signature of human airway epithelium as it undergoes full differentiation into mucociliated epithelial cells under air-liquid interface. We used microarrays to detail the global gene expression pattern from day 0 through day 28 following air-liquid interface in human airway epithelial cells and identified distinct clusters of gene expression during this process.

2022-11-14 | GSE197142 | GEO

Direct exposure to SARS-CoV-2 and cigarette smoke increases infection severity and alters the stem cell-derived airway repair response

Project description:To study the effect of cigarette smoke exposure on Sars-Cov2 infection, we directly exposed mucociliary air-liquid interface (ALI) cultures derived from primary human nonsmoker airway basal stem cells (ABSCs) to short term cigarette smoke and infected them with live SARS-CoV-2. We set out to examine the underlying mechanisms governing the increased susceptibility of cigarette smoke exposed ALI cultures to SARS-CoV-2 infection by usingle cell profiling of the cultures, which showed that interferon response genes were induced in SARS-CoV-2 infected airway epithelial cells in ALI cultures but smoking exposure together with SARS-CoV-2 infection reduced the interferon response.

2020-11-17 | GSE161089 | 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