Gene expression profiles of nasal epithelium in long COVID and post-COVID
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1209122 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR31990340_1.fastq.gz | Fastqsanger.gz | |||
| SRR31990340_2.fastq.gz | Fastqsanger.gz | |||
| SRR31962386_1.fastq.gz | Fastqsanger.gz | |||
| SRR31962386_2.fastq.gz | Fastqsanger.gz | |||
| SRR31962387_1.fastq.gz | Fastqsanger.gz |
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Project description:Recent studies suggest that chronic inflammation and immune dysregulation in the local tissues and systemically play a critical role in the pathophysiology of long COVID. Here, we report a role for nasal epithelium in mediating inflammation in a subset of long COVID patients. We demonstrate impaired barrier function of nasal epithelial cells, inadequate wound healing potential, and nasal cell hypersensitivity along with a persistent inflammatory state in long COVID. These inflamed structural cells activate type 1 innate lymphoid cells in the blood of long COVID patients and propagate systemic inflammation. We demonstrated the importance of understanding the immunological mechanisms driving long COVID to develop effective treatments. We highlight the critical role of the nasal epithelial barrier and the interplay between epithelial cells and ILCs in maintaining mucosal homeostasis and contributing to chronic inflammation in long COVID.
2025-01-31 | GSE286429 | GEO
Project description:Background: Post-COVID syndrome (PCS) currently affects approximately 3-17% of people following severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and has the potential to become a significant global health burden. While PCS exhibits diverse symptoms, improved assessment methods are being developed to guide therapy. Despite this, there is a lack of mechanistic insights and treatment options. Objective: To elucidate molecular mechanisms underlying PCS by employing single-cell RNA transcriptomics on patients’ nasal tissue and in vitro validation. Methods: Single-cell RNA transcriptomic analysis was conducted on nasal biopsies from 25 PCS patients with moderate or severe PCS symptoms. Identification of cell types, signaling, and cell-cell communication was performed. In vitro, air-liquid interface cultures were employed to validate findings, with a particular focus on the TNFα-TGFβ axis. Results: Severe PCS was associated with reduced numbers of ciliated cells, increased immune cell presence, and inflammatory signaling leading to TGFβ and TNFα upregulation, all without any viral load. This induced an epithelial-mesenchymal transition, increasing basal cell abundance and a mis-stratified nasal epithelium. In vitro experiments validated TGFβ and TNFα as causal cytokines promoting the reduced abundance of ciliated epithelium and expansion of basal epithelial cells. As such, we posit that a sustained severe PCS phenotype was not linked to continued viral load but instead to immune cell presence and persistent cytokine production. Conclusions: Our study reveals a pathway for persistent severe PCS involving immune-mediated nasal tissue damage, suggesting therapeutic potential by targeting the TNFα-TGFβ axis. The restoration of the nasal epithelium may prove to be a possible treatment strategy for PCS, akin to interventions in other chronic inflammatory conditions.
2025-06-16 | GSE299529 | 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.
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Project description:scRNA-seq reveals persistent aberrant differentiation of nasal epithelium driven by TNFα and TGFβ in post-COVID syndrome
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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.
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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:COVID-19 symptoms range from mild to severe illness; the cause for this differential response to infection remains unknown. Unraveling the immune mechanisms acting at different levels of the colonization process might be key to understand these differences. We carried out a multi-tissue (nasal, buccal and blood) gene expression analysis of immune-related genes from patients affected by different COVID-19 severities, and healthy controls.
2021-12-31 | GSE183071 | GEO
Project description:Understanding on pathogenesis of COVID-19 is rapidly growing, but primary target cells of SARS-CoV-2 infection is still not known. Here, we performed single cell RNA sequencing on human nasal swab from COVID-19 patient to investigate the expression patterns of host cell entry factors of SARS-CoV-2.
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Project description:Generation of single cell and single nuclei transcriptomic data of post-mortem tissues from a Malawi cohort. We aim to explore differences in the immune response between Covid-19, Non-Covid19 LRTD (lower respiratory tract disease) and no-LTRD at the single cell level from lung, nasal and blood. Autopsies were conducted through minimally invasive autopsy using needle-biopsy. Samples were then processed with a 10X Chromium in Blantyre, Malawi. Some samples were run individually and others pooled. Pooled samples were split using single nucleotide polymorphisms or through hashtag oligonucelotides. Data processing and analysis was performed in R using the Seurat package.
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Project description:Post-acute sequelae of COVID-19 (PASC) represent an emerging global crisis. However, quantifiable risk-factors for PASC and their biological associations are poorly resolved. We executed a deep multi-omic, longitudinal investigation of 309 COVID-19 patients from initial diagnosis to convalescence (2-3 months later), integrated with clinical data, and patient-reported symptoms. We resolved four PASC-anticipating risk factors at the time of initial COVID-19 diagnosis: type 2 diabetes, SARS-CoV-2 RNAemia, Epstein-Barr virus viremia, and specific autoantibodies. In patients with gastrointestinal PASC, SARS-CoV-2-specific and CMV-specific CD8+ T cells exhibited unique dynamics during recovery from COVID-19. Analysis of symptom-associated immunological signatures revealed coordinated immunity polarization into four endotypes exhibiting divergent acute severity and PASC. We find that immunological associations between PASC factors diminish over time leading to distinct convalescent immune states. Detectability of most PASC factors at COVID-19 diagnosis emphasizes the importance of early disease measurements for understanding emergent chronic conditions and suggests PASC treatment strategies.
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