Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA210252 | ENA |
REPOSITORIES: ENA
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Project description:We used microarrays to compare the gene expression profiles of different H1N1 isolates (seasonal and pandemic) in lung epithelial cells in vitro. Well-differentiated primary human lung, bronchial epithelial cells (wd-NHBE) were infected with two pandemic and one seasaonl H1N1 influenza viruses at a multiplicity of infection of 3.0. The cells were then collected, in triplicate, at 36 hours after infection. This timepoint was selected as we saw significant differences in soluble cytokine and chemokine protein levels at this time point in the supernatant.
2013-07-03 | E-GEOD-48466 | biostudies-arrayexpress
Project description:Lung infection by influenza A viruses is a common cause of disease exacerbations in patients with chronic obstructive pulmonary disease (COPD), however, this process is difficult to study in human patients. Here we used a microfluidic human lung airway-on-a-chip (Airway Chip) lined by primary human bronchial epithelium interfaced with primary human pulmonary microvascular endothelium to model this process in vitro. Airway Chips containing bronchial epithelial cells from COPD patients successfully replicated the increased sensitivity to the lung airway to infection by both influenza H1N1 and H3N2 viruses compared to chips lined by epithelium from healthy donors, including enhanced viral loads and increased production of inflammatory cytokines. Transcriptomics analysis of the healthy and COPD epithelium following infection with influenza H1N1 virus on-chip resulted in identification of several novel markers of COPD
2022-04-01 | GSE186908 | GEO
Project description:Pandemic influenza H1N1 (pdmH1N1) virus causes mild disease in humans but occasionally leads to severe complications and even death, especially in those who are pregnant or have underlying disease. Cytokine responses induced by pdmH1N1 viruses in vitro are comparable to other seasonal influenza viruses, suggesting the cytokine dysregulation as seen in H5N1 infection is not a feature of the pdmH1N1 virus. However, a comprehensive gene expression profile of pdmH1N1 in relevant primary human cells in vitro has not been reported. Type I alveolar epithelial cells are a key target cell in pdmH1N1 pneumonia. We carried out a comprehensive gene expression profiling using the Affymetrix microarray platform to compare the transcriptomes of primary human alveolar type I-like alveolar epithelial cells infected with pdmH1N1 or seasonal H1N1 virus. Primary type II alveolar epithelial cells were isolated from human non-malignant lung tissue of three patients who underwent lung resection, and cells were differentiated to type I-like before use. Type I-like alveolar epithelial cells were mock infected, or infected with pdmH1N1 or seasonal H1N1 viruses at a multiplicity of infection (MOI) of two. Total RNA was extracted from cells after 8h post-infection, and gene expression profiling was performed using an Affymetrix Human Gene 1.0 ST microarray platform.
2010-10-06 | E-GEOD-24533 | biostudies-arrayexpress
Project description:In this study, we performed a miRNA global profiling in human lung epithelial cells (A549) infected by two different subtypes of human influenza A viruses (H1N1 and H3N2).
2013-04-03 | GSE42003 | GEO
Project description:Pandemic H1N1 influenza A (H1N1pdm) elicits stronger pulmonary inflammation than previously circulating seasonal H1N1 influenza A (sH1N1), yet mechanisms of inflammatory activation in respiratory epithelial cells during H1N1pdm infection are unclear. We investigated host responses to H1N1pdm / sH1N1 infection and virus entry mechanisms in primary human bronchial epithelial cells in vitro. H1N1pdm infection rapidly initiated a robust inflammatory gene signature (3 h post-infection) not elicited by sH1N1 infection. Protein secretion inhibition had no effect on gene induction. Infection with membrane fusion deficient H1N1pdm failed to induce robust inflammatory gene expression which was rescued with restoration of fusion ability, suggesting H1N1pdm directly triggered the inflammatory signature downstream of membrane fusion. Investigation of intra-virion components revealed H1N1pdm viral RNA (vRNA) triggered a stronger inflammatory phenotype than sH1N1 vRNA. Thus, our study is first to report H1N1pdm induces greater inflammatory gene expression than sH1N1 in vitro due to direct virus-epithelial cell interaction. Total RNA obtained from Normal Human Bronchial Epithelial Cells (NHBEC) at 3 hours or 24 hours post-infection with either 0.9 MOI A/Mexico/4108/2009 (H1N1) or 0.9 MOI A/Brisbane/59/2007 (H1N1). Total RNA was also collected at 0 hours from uninfected NHBEC for each infection. Changes in gene expression relative to uninfected cells were then investigated.
2016-07-04 | E-GEOD-48575 | biostudies-arrayexpress
Project description:A comparative gene expression analysis was performed using cDNA microarray technology in passage-2 normal human nasal epithelial cells to identify the differentially expressed genes between influenza A virus infected and uninfected cells. Two samples were analyzed. RNA was extracted from normal human nasal epithelial cells, which were further divided as H1N1 PI 0 day and H1N1 PI 2 day (influenza A virus infection for 48 hr).
2013-05-02 | E-GEOD-46567 | biostudies-arrayexpress
Project description:This study used virological, histological, immunological and global gene expression to compare the virlence of two newly emerged 2009 H1N1 isolates (A/Mexico/InDRE4487/2009 and A/Mexico/4108/2009) and current seasonal H1N1 influenza strain (A/Kawasaki/UTK-4/2009) in experimentally infected cynomolgus macaques. We showed that infection of macaques with two genetically similar but clinically distinct SOIV isolates from the early stage of the pandemic (A/Mexico/4108/2009 and A/Mexico/InDRE4487/2009) resulted in upper and lower respiratory tract infections and clinical disease ranging from mild to severe pneumonia. Disease associated with these SOIV isolates was clearly advanced over the mild infection caused by A/Kawasaki/UTK-4/2009, a current seasonal strain.
2011-08-30 | GSE31694 | GEO
Project description:We defined the major transcriptional responses in primary human bronchial epithelial cells (HBECs) after either infection with influenza or treatment with relevant ligands. We used four different strategies, each highlighting distinct aspects of the response. (1) cells were infected with the wild-type PR8 influenza virus that can mount a complete replicative cycle. (2) cells were transfected with viral RNA (âvRNAâ) isolated from influenza particles. This does not result in the production of viral proteins or particles and identifies the effect of RNA-sensing pathways (e.g., RIG-I.). (3) Cells were treated with interferon beta (IFNb), to distinguish the portion of the response which is mediated through Type I IFNs. (4) Cells were infected with a PR8 virus lacking the NS1 gene (âDNS1â). The NS1 protein normally inhibits vRNA- or IFNb-induced pathways, and its deletion can reveal an expanded response to infection. HBECs were stimulated with a 15 minute pulse of 1000U/ml IFNÃ (PBL, Piscataway, NJ), 100ng/ml vRNA (purified directly from PR8 virus) with LTX transfection reagent (Invitrogen; Carlsbad, California), wild type H1N1 influenza (A/PR/8/34) or ?NS1 virus (PR8 with a deleted NS1 gene, gift from Dr. Garcia-Sastre). Viruses were used at a multiplicity of infection (moi) of 5. Control samples were incubated with media or LTX under the same conditions. Cells were washed, supplemented with warm media and harvested at 11 timepoints (0, .25, .5, 1, 1.5, 2, 4, 6, 8, 12, and 18 hours post-treatment). HBECs were seeded in 6 well plates at a concentration of 250,000/well 18 hours prior to stimultaion. Cells were stimulated with a 15 minute pulse of IFNb, vRNA, infected with PR8 influenza or NS1 deleted influenza, or mock treated
2010-04-13 | E-GEOD-19392 | biostudies-arrayexpress
Project description:Transcriptome profiling of influenza virus-infected human bronchial epithelial cells
| PRJNA305099 | ENA
Project description:Differential expression was determined in Calu-3 cells between mock infected and infected with H1N1 influenza virus A/Netherlands/602/2009 at nine time points post-infection. As a comparison, cells were also infected with A/CA/04/2009 H1N1 influenza virus at 4 time points post-infection.
2012-09-13 | GSE40844 | GEO