Club cells surviving influenza A virus infection induce temporary non-specific anti-viral immunity
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA311328 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR3157720.fastq.gz | Fastqsanger.gz | |||
| SRR3157730.fastq.gz | Fastqsanger.gz | |||
| SRR3157740.fastq.gz | Fastqsanger.gz | |||
| SRR3157750.fastq.gz | Fastqsanger.gz | |||
| SRR3157721.fastq.gz | Fastqsanger.gz |
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Project description:Cells respond differently to influenza virus infection after already having been infected previously. Anlysis of cellular RNA after influenza virus infection
2016-03-01 | E-GEOD-77734 | biostudies-arrayexpress
Project description:Cells respond differently to influenza virus infection after already having been infected previously.
2016-03-01 | GSE77734 | GEO
Project description:A brief window of antigen-nonspecific protection has been observed after influenza A virus (IAV) infection. Although this temporary immunity has been assumed to be the result of residual nonspecific inflammation, this period of induced immunity has not been fully studied. Because IAV has long been characterized as a cytopathic virus (based on its ability to rapidly lyse most cell types in culture), it has been a forgone conclusion that directly infected cells could not be contributing to this effect. Using a Cre recombinase-expressing IAV, we have previously shown that club cells can survive direct viral infection. We show here not only that these cells can eliminate all traces of the virus and survive but also that they acquire a heightened antiviral response phenotype after surviving. Moreover, we experimentally demonstrate temporary nonspecific viral immunity after IAV infection and show that surviving cells are required for this phenotype. This work characterizes a virally induced modulation of the innate immune response that may represent a new mechanism to prevent viral diseases.
| S-EPMC4833272 | biostudies-literature
Project description:Gene expression patterns of bronchiolar progenitors and club cells in mouse lung were examined by microarray experiments. Although it has not yet been fully characterized, a subset of epithelial cells lining bronchioles are best understood as bronchiolar progenitors that self-renew over the long term and that can differentiate into more differentiated club cells and ciliated cells. The bronchiolar progenitors are distinct from club cells and characteristically express the alveolar type 2 cell marker, prosurfactant protein C, with lower levels of club cell secretory protein/Scgb1a1. There are also functional differences between them; while club cells can be depleted by naphthalene because of the abundance of cytochrome P450 enzyme Cyp2f2, bronchiolar progenitors are resistant to naphthalene-induced depletion because of defects in the enzyme.
2016-02-17 | E-MTAB-4460 | biostudies-arrayexpress
Project description:Lung adenocarcinoma (LUAD) is one of the deadliest malignancies worldwide. Dynamic lineage changes within the lung epithelium and the high plasticity of these epithelial cells confound the correct identification of the cell-of-origin of LUAD. Here, we combined lineage-tracing mouse models with an autochthonous cell type-independent LUAD model in order to discover the cellular origin of ALK-translocated LUAD. We identified Club and AT2 cells as the cells-of-origin of LUAD. Moreover, we uncovered epigenetic imprints in the tumours originating from Club or AT2 cells by whole-genome bisulfite sequencing. Single-cell transcriptomes of Club cells at different stages of tumour development identified two trajectories of Club cell evolution. On both routes, tumours lose their Club cell identity and gain an AT2-like phenotype. Together, this study highlights the role of Club cells in LUAD initiation and unveils key mechanisms conferring LUAD heterogeneity.
2022-06-30 | GSE176185 | GEO
Project description:Lung adenocarcinoma (LUAD) is one of the deadliest malignancies worldwide. Dynamic lineage changes within the lung epithelium and the high plasticity of these epithelial cells confound the correct identification of the cell-of-origin of LUAD. Here, we combined lineage-tracing mouse models with an autochthonous cell type-independent LUAD model in order to discover the cellular origin of ALK-translocated LUAD. We identified Club and AT2 cells as the cells-of-origin of LUAD. Moreover, we uncovered epigenetic imprints in the tumours originating from Club or AT2 cells by whole-genome bisulfite sequencing. Single-cell transcriptomes of Club cells at different stages of tumour development identified two trajectories of Club cell evolution. On both routes, tumours lose their Club cell identity and gain an AT2-like phenotype. Together, this study highlights the role of Club cells in LUAD initiation and unveils key mechanisms conferring LUAD heterogeneity.
2022-06-30 | GSE176184 | GEO
Project description:The club cell, a small airway epithelial (SAE) secretory cell that uniquely expresses SCGB1A1, plays a central role in host defense in the human lung. Based on data demonstrating that ~50% of club cells express MUC5B, a secretory mucin critical for mucociliary clearance, we hypothesized that subpopulations of club cells with distinct functions may exist. To evaluate this, the SAE of normal nonsmokers and healthy cigarette smokers was sampled by bronchoscopy and brushing followed by single cell sequencing using Drop-seq technology. Subpopulations of SCGCB1A1+KRT5loMUC5AC- club cells were assessed by unsupervised clustering to evaluate club cell subpopulations. Immunostaining of SAE in lung sections, brushed SAE cells, and in vitro air-liquid interface culture was utilized to confirm the transcriptomic-based observations. Unsupervised clustering of SCGCB1A1+KRT5loMUC5AC‾ club cells in the SAE identified 3 unique club cell populations that differed by differentiation state and function, including: (1) progenitor; (2) proliferating; and (3) effector subpopulations. The progenitor club cell population was energetically active with high expression of mitochondrial and ribosomal proteins and the highest KRT5 levels vs other club cell populations. The proliferating population, defined by high expression of cyclins and proliferation markers, was the smallest, representing 2% of club cells. The effector club cell cluster expressed transcripts for host defense genes, xenobiotic metabo-lism, and barrier functions commonly associated with club cell function. Comparison of the club cell subpopulations in smokers vs nonsmokers demonstrated that the proportion of the club cell effector population was significantly decreased in smokers with a concomitant significant in-crease in the proliferating cell population. These observations provide novel insights into both the makeup of human SAE club cell subpopulations and smoking-induced changes in club cell biology.
2021-09-22 | GSE155515 | GEO
Project description:Background and objective: The role of bronchiolar epithelial cells in the pathogenesis of pulmonary fibrosis has not been addressed. We previously demonstrated that DNA damage was found in bronchiole at early phase, and subsequently extended to alveolar cells at later phase in bleomycin-induced pulmonary fibrosis in mice. Club cells are progenitor cells for bronchiole, and are recognized to play protective roles against lung inflammation and damage. The aim of the study was to elucidate the role of club cells in the development of pulmonary fibrosis. Methods: C57BL/6J mice were received naphthalene intraperitoneally at day -2 to deplete club cells, and were given intratracheal bleomycin or vehicle at day 0. Lung tissues were obtained at day 1, 7, and 14, and bronchoalveolar lavage was performed at day 14. Gene expression was analysed from bronchiolar ephithelial cells sampled by laser captured microdissection at day 14. Results: Surprisingly, naphthalene-induced club cell depletion protected mice from bleomycin-induced lung injury and fibrosis. We conclude that club cells are involved in the development of lung injury and fibrosis.
2017-02-08 | GSE94522 | GEO
Project description:Rationale: The role of club cells in the pathology of Idiopathic Pulmonary Fibrosis IPF is not well understood. PDIA3, an endoplasmic reticulum (ER) based redox chaperone catalyzes the cysteine disulfide bonds (-S-S-) in various fibrosis-related proteins; however, mechanisms of action of PDIA3 in pulmonary fibrosis is not fully elucidated. Objectives: To examine the role of club cells and PDIA3 in the pathogenesis of pulmonary fibrosis (PF) and therapeutic potential of inhibition of PDIA3 in PF. Methods: The impact of PDIA3 and aberrant club cells in PF was studied by retrospective analysis of human transcriptome data from LGRC, and specific deletion and inhibition of PDIA3 in club cells and blocking Osteopontin (SPP1) downstream of PDIA3 in mice. Measurements and Main Results: The PDIA3 along with club cell secretory protein (SCGB1A1 or CCSP) signatures are upregulated in IPF compared to control patients, and PDIA3 increases correlate with a decrease in lung function in IPF patients. The Bleomycin (BLM) model of PF showed increases in aberrant CCSP and PDIA3 positive cells in the lung parenchyma. Ablation of Pdia3, specifically in CCSP cells, decreases CCSP cells along with PF in mice. The therapeutic administration of a PDI inhibitor LOC14 reversed the BLM-induced CCSP cells and PF in mice. The proteomic screen of the PDIA3 partners revealed SPP1 as a major interactor in PF. Blocking SPP1 attenuated the development of PF in mice. Conclusions: Collectively, this study demonstrates a new relationship of club cells, with PDIA3, SPP1, and a putative pathological function of club cells in pulmonary fibrosis.
2021-11-11 | PXD021715 | Pride
Project description:Club (“Clara”) cells, dome shaped cells with disease cytoplasmic granules and microvilli, are the major secretory cell of the human small (>6 generation) airways. Little is known regarding the biology of club cells in the human airway, nor of the ontogeny of this cell type. Taking advantage of the SCGB1A1 as the marker for club cells and our ability to sample the normal small airway epithelium by bronchoscopy and brushing healthy volunteers, we defined the transcriptome of the normal human airway club cell using single cell transcriptome sequencing. Analysis of the human small airway epithelial single cell transcriptome together with in vitro validation provides novel insights into the molecular phenotype and biological functions of the human club cell population and identifies the basal cell as the human progenitor cells for club cells.
2024-06-05 | GSE94819 | GEO