Host transcription profile in nasal epithelium and blood of hospitalized children under two years old with Respiratory Syncitial Virus infection
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PROVIDER: PRJNA382796 | ENA |
REPOSITORIES: ENA
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Project description:Analysis of transcriptional profiles in whole blood and nasopharyngeal swaps from children hospitalized with lower respiratory tract infections at their admission and their discharge, and diagnosed with either RSV or rhinovirus infections. The hypothesis is that this information will contribute to better understand the viral specific immunity and host responses to RSV infection and may suggest leads for the develoment of vaccines and specific treatment.
2017-04-14 | GSE97742 | GEO
Project description:Analysis of transcriptional profiles in whole blood and nasopharyngeal swaps from children hospitalized with lower respiratory tract infections at their admission and their discharge, and diagnosed with either RSV or rhinovirus infections. The hypothesis is that this information will contribute to better understand the viral specific immunity and host responses to RSV infection and may suggest leads for the develoment of vaccines and specific treatment.
2017-04-14 | GSE97741 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2017-04-14 | GSE97743 | GEO
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
Project description:The nasal epithelium is an important target site for chemically-induced toxicity and carcinogenicity. Human epidemiological investigations and experimental laboratory animal studies show that the nasal olfactory epithelium is selectively damaged by inhalation exposure to several chemicals, including vinyl acetate and hydrogen sulfide. The reason for the relative sensitivity of the nasal olfactory epithelium is not known. To better understand and predict the response of the nasal epithelium to inhaled xenobiotics, gene expression profiles from naÑve male and female Sprague-Dawley rats were constructed. Epithelial cells were manually collected from the nasal septum, naso- and maxillo-turbinates, and ethmoid turbinates of 9 male and 9 female rats. Gene expression analysis was performed using the Affymetrix Rat Genome 430 2.0 microarray. Gene ontology enrichment analysis identified several functional categories including xenobiotic metabolism, cell cycle, apoptosis, and ion channel/transport with significantly different expression between tissue types. Surprisingly, there were few gender differences in gene expression. This baseline data will contribute to our understanding of the normal physiology and selectivity of the nasal epithelial cellsâ response to inhaled environmental toxicants. Experiment Overall Design: To better understand and predict the response of the nasal epithelium to inhaled xenobiotics, gene expression profiles from naÑve male and female Sprague-Dawley rats were constructed. Epithelial cells were manually collected from the nasal septum, naso- and maxillo-turbinates, and ethmoid turbinates of 9 male and 9 female rats. Gene expression analysis was performed using the Affymetrix Rat Genome 430 2.0 microarray.
2008-06-13 | E-GEOD-5019 | biostudies-arrayexpress
Project description:The nasal epithelium is an important target site for chemically-induced toxicity and carcinogenicity. Human epidemiological investigations and experimental laboratory animal studies show that the nasal olfactory epithelium is selectively damaged by inhalation exposure to several chemicals, including vinyl acetate and hydrogen sulfide. The reason for the relative sensitivity of the nasal olfactory epithelium is not known. To better understand and predict the response of the nasal epithelium to inhaled xenobiotics, gene expression profiles from naїve male and female Sprague-Dawley rats were constructed. Epithelial cells were manually collected from the nasal septum, naso- and maxillo-turbinates, and ethmoid turbinates of 9 male and 9 female rats. Gene expression analysis was performed using the Affymetrix Rat Genome 430 2.0 microarray. Gene ontology enrichment analysis identified several functional categories including xenobiotic metabolism, cell cycle, apoptosis, and ion channel/transport with significantly different expression between tissue types. Surprisingly, there were few gender differences in gene expression. This baseline data will contribute to our understanding of the normal physiology and selectivity of the nasal epithelial cells’ response to inhaled environmental toxicants. Keywords: Comparative
2007-05-01 | GSE5019 | GEO
Project description:The nasal epithelium represents the first line of defense against inhaled pathogens, allergens, and irritants and plays a key role in the pathogenesis of a spectrum of acute and chronic airways diseases. Despite age-dependent clinical phenotypes triggered by these noxious stimuli, little is known about how ageing affects the structure and function of the airway epithelium that is crucial for lung homeostasis and host defense. The aim of this study was therefore to determine age-related differences in structural and functional properties of primary nasal epithelial cultures from healthy children and non-smoking elderly people. To achieve this goal, highly differentiated nasal epithelial cultures were established from nasal brushes at air-liquid-interface and used to study epithelial cell type composition, mucin (MUC5AC and MUC5B) expression and ion transport properties. Further, we determined age-dependent molecular signatures using global proteomic analysis. We found lower numeric densities of ciliated cells and higher levels of MUC5AC expression in cultures from children vs. elderly people. Bioelectric studies showed no differences in basal ion transport properties, ENaC-mediated sodium absorption or CFTR-mediated chloride transport, but detected decreased calcium-activated TMEM16A-mediated chloride secretory responses in cultures from children vs. elderly people. Proteome analysis identified distinct age-dependent molecular signatures associated with ciliation and mucin biosynthesis, as well as other pathways implicated in ageing. Our data identified intrinsic, age-related differences in structure and function of the nasal epithelium and provide a basis for further studies on the role of these findings in age-dependent airways disease phenotypes observed with a spectrum of respiratory infections and other noxious stimuli.
2022-02-28 | PXD030130 | Pride
Project description:Smoking is the leading cause of lung cancer death, although only a small percentage of smokers develop the disease. Cigarette smoke exposure is known to cause a field of injury in cells throughout the respiratory tract, and while these airway epithelial cells are morphologically normal, they can undergo genetic alterations in response to cigarette smoke exposure. We used microarrays to analyze the gene expression of epithelial cells in the extrathoracic epithelium, specifically nasal and buccal epithelium, to see if these cells underwent similar genetic alterations in response to tobacco exposure as seen in bronchial epithelial cells as has been previously reported. Experiment Overall Design: Buccal and nasal epithelial cell samples were collected from healthy current and never smokers. RNA was isolated from these samples and hybridized to Affymetrix microarrays. Gene expression from never smokers was compared to never smoker gene expression from bronchial epithelium as well as expression data from other tissues to determine commonalities in expression patterns in normal extra- and intra-thoracic samples. In addition, gene expression from smokers and nonsmokers was compared in bronchial, nasal, and buccal epithelium to determine similarities in gene expression in these tissues in response to cigarette smoker exposure.
2008-10-20 | E-GEOD-8987 | biostudies-arrayexpress
Project description:Background: In asthma, airway epithelium remodeling can already be detected during childhood, and epithelial cells are more susceptible to virus and oxidative stress. Their exact role in natural history and severity of children allergic respiratory disease remains however surprisingly unexplored. Aim: To analyze dysfunctions of epithelium in dust mite allergic respiratory disease (rhinitis ± asthma) in children. Methods: Expression profilings of nasal epithelial cells collected by brushing were performed on Affymetrix Hugene 1.0 ST arrays. All allergic patients were sensitized to dust mite. 19 patients had an isolated allergic rhinitis (AR). 14 patients had AR associated with asthma. Patients were compared to 12 controls, their severity and control being assessed according to NAEPP and ARIA criteria. Infections by respiratory viruses were excluded by real-time PCR measurements. Results: 61 probes were able to distinguish allergic rhinitis children from healthy controls. A majority of these probes was under the control of Th2 cytokines, as evidenced by parallel experiments performed on primary cultures of nasal epithelial cells. In uncontrolled asthmatic patients, we observed not only an enhanced expression of these Th2-responsive transcripts, but also a down-regulation of interferon-responsive genes. Conclusion: Our study identifies a Th2 driven epithelial phenotype common to all dust mite allergic children. Besides, it suggests that epithelium is involved in the severity of the disease. Expression profiles observed in uncontrolled asthmatic patients suggest that severity of asthma is linked at the same time to atopy and to impaired viral response. Nasal epithelium gene expression profiling of dust mite allergic children with isolated rhinitis, rhinitis associated with asthma and controls. 38 samples classified in 4 categories : 14 isolated rhinitis (R), 6 rhinitis with uncontrolled asthma (UA), 7 rhinitis with controlled asthma (CA) and 11 healthy subjects (C )
2012-01-05 | E-GEOD-19187 | biostudies-arrayexpress
Project description:Cystic Fibrosis Nasal Epithelium Gene Expression by RNAseq
| PRJNA671149 | ENA