Circadian regulation of SARS-CoV-2 infection in lung epithelial cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE176393 | GEO | 2021/10/12
REPOSITORIES: GEO
Similar Datasets
Project description:SARS-CoV-2, the virus responsible for COVID-19, infects both human airway epithelial cells and trigeminal ganglia. We assessed the consequences of SARS-CoV-2 infection on gene expression in Calu-3 cells and in primary Mus musculus trigeminal ganglia cells (mmTG). Here, we provide datasets that include raw reads and mapped reads for the following: 1) mock infected mmTG 48 hrs post infection; 2) SARS-CoV-2 infected mmTG 48 hrs post infection; 3) mock infected Calu-3 cells 24 hrs post infection; 4) SARS-CoV-2 infected Calu-3 cells 24 hrs post infection; 5) mock infected Calu-3 cells 48 hrs post infection; 6) SARS-CoV-2 infected Calu-3 cells 48 hrs post infection.
2024-01-08 | GSE252056 | GEO
Project description:Fah-/-, Rag2-/-, IL2Rg-/-, non-obese diabetic (FRG-NOD) mice transplanted with primary human hepatocytes were infected with 10^9 HBV genome equivalents purified from concentrated supernatant of the HepG2.2.15 cell line (HBV genotype D subtype ayw). Eight weeks later mice were treated twice a day by intraperitoneal injection of either vehicle or 100 mg/kg SR9009 for 2 weeks. At the end of experiment, mouse livers were collected for RNA-seq analysis. The sequence reads were mapped to the human or mouse genome.
2020-12-16 | GSE163285 | GEO
Project description:The goals of this study are to dmonstrate transcriptomic profiling of SARS-CoV-2 infected brain samples. Hippocampal mRNA profiles of hACE2 transgenic mice at 30-day post SARS-CoV-2 infection were generated by bulk RNA sequencing, in 3 samples each group. Sequence reads were mapped to the mouse genome (GRCm38) using STAR. RSEM was used to count aligned reads that mapped to the annotated mouse genes. Gene-level differential expression analyses were performed using R package DESeq2. Results showed that SARS-CoV-2 infection led to long-term effect regarding neuroinflammation and neuronal function.
2022-09-30 | GSE199545 | GEO
Project description:Severe acute respiratory syndrome-associated coronavirus (SARS-CoV) infection causes an immune-mediated disease. We have recently shown that SARS-CoV-induced epithelial Calu-3 cytokines could exacerbate and dampen host inflammatory and T cell responses, respectively, through modulating the functions of macrophages and dendritic cells, thereby suggesting that not only are lung epithelial cells the primary cells of SARS-CoV infection, but they also involve in initiating and orchestrating the host innate and adaptive immunity. Comprehensive evaluation of the complex epithelial signaling to SARS-CoV is, thus, crucial for paving the way to better understand SARS pathogenesis and develop the innovative therapeutics against SARS. Here, based on the microarray-based functional genomics, we reported that 2B4 cells, a clonal derivative of Calu-3 cells, elicited a temporal and spatial activation of nuclear factor (NF)kappaB, activator protein (AP)-1 (ATF2/c-Jun), and interferon regulatory factor (IRF)-3/-7 at 12-, 24-, and 48-hrs post infection (p.i.), respectively, resulting in the activation of many antiviral genes, including interferon (IFN)-β, -λs, SARS-related inflammatory mediators, and various IFN-stimulated genes (ISGs). While elevated responses of IFN-β and IFN-λs were not detected until 48-hrs p.i., as a consequence of a delayed IRF-3/-7 activation, we showed, for the first time, that both types of IFNs exerted previously under-described non-redundant, complementary, and/or synergistic effects on the epithelial defense against SARS-CoV. Collectively, our results highlight the molecular mechanisms of the sequential activation of virus- and IFN-dependent signaling of lung epithelial cells against SARS-CoV and identify novel cellular targets for future studies, aiming at advancing strategies against SARS.
2010-02-01 | GSE17400 | GEO
Project description:We performed RNA sequencing of Calu-3 cells after treatment with the BET-domain inhibitors JQ-1 and ABBV-744 as well as BRD2 CRISPRi knockdown. We also included CRISPRi knockdown of two other validated hit genes from our screen, COMP and ACE2.
2021-01-19 | GSE165025 | GEO
Project description:Severe acute respiratory syndrome-associated coronavirus (SARS-CoV) infection causes an immune-mediated disease. We have recently shown that SARS-CoV-induced epithelial Calu-3 cytokines could exacerbate and dampen host inflammatory and T cell responses, respectively, through modulating the functions of macrophages and dendritic cells, thereby suggesting that not only are lung epithelial cells the primary cells of SARS-CoV infection, but they also involve in initiating and orchestrating the host innate and adaptive immunity. Comprehensive evaluation of the complex epithelial signaling to SARS-CoV is, thus, crucial for paving the way to better understand SARS pathogenesis and develop the innovative therapeutics against SARS. Here, based on the microarray-based functional genomics, we reported that 2B4 cells, a clonal derivative of Calu-3 cells, elicited a temporal and spatial activation of nuclear factor (NF)kappaB, activator protein (AP)-1 (ATF2/c-Jun), and interferon regulatory factor (IRF)-3/-7 at 12-, 24-, and 48-hrs post infection (p.i.), respectively, resulting in the activation of many antiviral genes, including interferon (IFN)-β, -λs, SARS-related inflammatory mediators, and various IFN-stimulated genes (ISGs). While elevated responses of IFN-β and IFN-λs were not detected until 48-hrs p.i., as a consequence of a delayed IRF-3/-7 activation, we showed, for the first time, that both types of IFNs exerted previously under-described non-redundant, complementary, and/or synergistic effects on the epithelial defense against SARS-CoV. Collectively, our results highlight the molecular mechanisms of the sequential activation of virus- and IFN-dependent signaling of lung epithelial cells against SARS-CoV and identify novel cellular targets for future studies, aiming at advancing strategies against SARS. DNA microarrays were performed in the Molecular Genomics (MG) Core Facilities at UTMB. The detailed information about the procedures of microarray analysis has been posted on the MG Core Facilities website (genomics@scms.utmb.edu). To characterize the dynamic, spatial, and temporal changes of the gene expression induced by SARS-CoV, confluent 2B4 cells grown in T-75 flasks were infected with SARS-CoV (MOI=0.1) or remained uninfected (as control) for 12, 24, and 48hrs. Because 2B4 cells were also permissive to the productive infection of Dhori virus (DHOV), a member of the Orthomyxoviridae family within the Thogotovirus genus, resulting in robust responses of IFNs and other pro-inflammatory mediators, we also established parallel cultures of DHOV-infected 2B4 cells (MOI=0.1) for the comparative analysis of global gene expression elicited by SARS-CoV- versus DHOV-infected 2B4 cells. To meet the minimal number required for application of statistical algorithms, we performed the study in triplicate at each time point for mock-, SARS-CoV-, and DHOV-infected cultures, yielding a total of 27 arrays. Briefly, supernatants were harvested from differentially treated cultures at 12-, 24-, and 48-hrs p.i. for subsequent analyses of viral yields and cytokine profiling, whereas the cells were subjected to total RNA extraction by using an RNAqueous-4PCR kit and following the protocol recommended by the manufacturer (Ambion, Austin, TX). Purified RNA samples were sent to our core facility for conversion to cDNA, biotin-labeled, and hybridized to 27 Affymetrix Human Genome U133 Plus 2.0 âGene Chipsâ each of which contained 54,675 probe set identifiers representing more than ~47,400 transcripts that identify ~38,500 well-characterized genes, and various internal controls (Affymetrix, Santa Clara, CA). Mock-infected cells were compared to cells infected with SARS-CoV or DHOV at each time point.
2010-02-24 | E-GEOD-17400 | biostudies-arrayexpress
Project description:Severe acute respiratory syndrome coronavirus-1 (SARS-CoV-1) and -2 (SARS-CoV-2) are beta-coronaviruses (β-CoVs) that have caused significant morbidity and mortality worldwide. Therefore, a better understanding of host responses to β-CoVs would provide insights into the pathogenesis of these viruses to identify potential targets for medical countermeasures. Our objective is to use a systems biology approach to explore the magnitude and scope of innate immune responses triggered by SARS-CoV-1 and -2 infection over time in pathologically relevant human lung epithelial cells (Calu-3/2B4 cells). Total RNA extracted at 12, 24, and 48 hours after β-CoVs infection of Calu-3/2B4 cells were subjected to RNA sequencing, bioinformatics, and functional enrichment analysis to select genes whose expressions were significantly modulated upon infection over time. The results of our study demonstrate that SARS-CoV-1 and -2 stimulate similar yet distinct innate antiviral signaling pathways in pathologically relevant human lung epithelial cells. Upregulated genes found at multiple time points regulated the viral life cycle, interferons, and interferon-stimulated genes (ISGs). Based on their profound modulation upon infection, we selected four ISGs, i.e., bone marrow stromal cell antigen 2 (BST2), Z-DNA Binding Protein 1 (ZBP1), C-X-C Motif Chemokine Ligand 11 (CXCL11), and Interferon Induced Transmembrane Protein 1 (IFITM1) for characterization as potential drug targets against β-CoVs.
2025-02-05 | GSE255647 | GEO
Project description:We used two model systems to characterise the changes caused by SARS-CoV-2 using quantitative proteomics. We used primary human epithelial cells differentiated at the air-liquid interface, first describing the relative abundance of proteins found in each major cell type of the epithelium, and then characterised the infection of ciliated cells specifically as these showed the greatest susceptibility to SARS-CoV-2 infection. We also used a lung epithelial cell line, CaLu-3, and compared the infection with B.29 and B.1.1.7 (Alpha) variant over a time-course of infection. In each case, immunostaining for nucleoprotein combined with FACS allowed for the purification of infected cells from uninfected ‘bystander’ cells.
2022-11-30 | PXD034101 | Pride
Project description:We used two model systems to characterise the changes caused by SARS-CoV-2 using quantitative proteomics. We used primary human epithelial cells differentiated at the air-liquid interface, first describing the relative abundance of proteins found in each major cell type of the epithelium, and then characterised the infection of ciliated cells specifically as these showed the greatest susceptibility to SARS-CoV-2 infection. We also used a lung epithelial cell line, CaLu-3, and compared the infection with B.29 and B.1.1.7 (Alpha) variant over a time-course of infection. In each case, immunostaining for nucleoprotein combined with FACS allowed for the purification of infected cells from uninfected ‘bystander’ cells.
2022-05-26 | PXD034135 | Pride
Project description:In the present study, we used data-independent acquisition mass spectrometry (DIA-MS) to analyse the protein expression in Calu-3 cells infected with SARS-CoV and SARS-CoV-2 over the time-course of 24 hours. About 8400 proteins were identified, from which about 90% could be quantified across the experiment. This results in a deep and comprehensive proteome map, which reflects time-dependent protein expression changes during SARS-CoV and SARS-CoV-2 infections and provides deep insights into the virus-specific immunmodulation of human lung cells.
2022-01-20 | PXD024883 | Pride