Nasal epithelium gene expression profiles from vaccinated or non-vaccinated humans challenged with influenza viruses
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PROVIDER: PRJNA1066769 | ENA |
REPOSITORIES: ENA
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Project description:Nasal epithelium gene expression profiles from vaccinated or non-vaccinated humans challenged with influenza viruses
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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.
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Project description:To explore the impact of nasal commensal viruses on the onset and progression of allergic rhinitis, We used single cell RNA sequencing (scRNA-seq) to analyze the diversity of CD45+ cells in the nasal mucosa of mice treated with Vehicle, Ribavirin, Vehicle-OVA, or Ribavirin-OVA.
2024-08-21 | GSE266238 | GEO
Project description:To elucidate the potential role of commensal viruses in the etiology of AR, we performed a metagenomic analysis of nasal lavage fluid (NLF) to identify commensal viruses in the nose of mice colonizing in the specific pathogen-free (SPF) circumstances (Vehicle group). To evaluate the potential role of these commensal viruses, we reduced them in the nose of mice by administrating intranasal drops of broad-spectrum antiviral drug ribavirin daily, starting at 4-week-old and lasting for three weeks (Ribavirin group).
2024-08-21 | GSE271863 | GEO
Project description:To elucidate the potential role of commensal viruses in the etiology of AR, we performed a metagenomic analysis of nasal mucosa to identify commensal viruses in the nose of mice. To evaluate the potential role of these commensal viruses in AR, we reduced them in the nose of mice by administrating intranasal drops of vehicle (Vehicle group) or broad-spectrum antiviral drug ribavirin daily, starting at 4-week-old and lasting for three weeks (Ribavirin group). These mice were also administrated with PBS, OVA, or HDM to induce AR.
2025-05-20 | GSE297096 | 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:For analyzing the exploratory nasal commensal viruses, we performed the metatranscriptomic analysis of the nose swabs from the enrolled AR patients both before and after treatments, as well as sequenced the nose swabs from a set of healthy volunteers without AR history.Simultaneously, to assess the expression of interferon-stimulated genes in patients with allergic rhinitis, we analyzed the gene expression of host reads.
2024-08-21 | GSE275114 | GEO
Project description:We examined the phenotypes and functions of SARS-CoV-2-specific T cells in the nasal mucosa of vaccinated individuals with breakthrough infection (BTI) or without infection.
2024-08-30 | GSE271754 | GEO
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:We isolated RNA from whole spleens of mice challenged with B. melitensis, some of which were vaccinated prior to infection.
2024-01-30 | GSE254248 | GEO