Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

MiRNA profiling in lung epithelial cells during infection with influenza A virus

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE44455 | GEO | 2013/03/01

SECONDARY ACCESSION(S): PRJNA190009

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

MiRNA profiling in lung epithelial cells during infection with influenza A virus

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-03-01 | E-GEOD-44455 | biostudies-arrayexpress

MiRNA profiling in lung epithelial cells during infection with influenza A virus of H5N1 strain

2013-03-01 | GSE44453 | GEO

MiRNA profiling in lung epithelial cells during infection with influenza A virus of H1N1 strain

2013-03-01 | GSE44452 | GEO

MiRNA profiling in lung epithelial cells during infection with influenza A virus of H1N1 strain

Project description:This study aims at elucidating how H1N1 influenza infection perturbs the host's miRNA regulatory pathways that may lead to adverse pathological events, such as cytokine storm, using the miRNA microarray approach. The cell line - NCI-H292, was infected with various preparations of H1N1 influenza viruses was analysed for miRNA expression profiles subsequently. The miRNA expression profiles were measured at 3, 6, 18, and 24 hours post infection, respectively.

2013-03-01 | E-GEOD-44452 | biostudies-arrayexpress

MiRNA profiling in lung epithelial cells during infection with influenza A virus of H5N1 strain

Project description:This study aims at elucidating how H5N1 influenza infection perturbs the host's miRNA regulatory pathways that may lead to adverse pathological events, such as cytokine storm, using the miRNA microarray approach. The cell line - NCI-H292, was infected with various preparations of H5N1 influenza viruses was analysed for miRNA expression profiles subsequently. The miRNA expression profiles were measured at 3, 6, 18, and 24 hours post infection, respectively.

2013-03-01 | E-GEOD-44453 | biostudies-arrayexpress

mRNA and miRNA analysis during hepatitis C virus infection

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-02-17 | E-GEOD-44370 | biostudies-arrayexpress

Transcriptomic profiling of a chicken lung epithelial cell line (CLEC213) reveals a mitochondrial respiratory chain activity boost during influenza virus infection.

Project description:Avian Influenza virus (AIV) is a major concern for the global poultry industry. Since 2012, several countries have reported AIV outbreaks among domestic poultry. These outbreaks had tremendous impact on poultry production and socio-economic repercussion on farmers. In addition, the constant emergence of highly pathogenic AIV also poses a significant risk to human health. In this study, we used a chicken lung epithelial cell line (CLEC213) to gain a better understanding of the molecular consequences of low pathogenic AIV infection in their natural host. Using a transcriptome profiling approach based on microarrays, we identified a cluster of mitochondrial genes highly induced during the infection. Interestingly, most of the regulated genes are encoded by the mitochondrial genome and are involved in the oxidative phosphorylation metabolic pathway. The biological consequences of this transcriptomic induction result in a 2.5- to 4-fold increase of the ATP concentration within the infected cells. PB1-F2, a viral protein that targets the mitochondria was not found associated to the boost of activity of the respiratory chain. We next explored the possibility that ATP may act as a host-derived danger signal (through production of extracellular ATP) or as a boost to increase AIV replication. We observed that, despite the activation of the P2X7 purinergic receptor pathway, a 1mM ATP addition in the cell culture medium had no effect on the virus replication in our epithelial cell model. Finally, we found that oligomycin, a drug that inhibits the oxidative phosphorylation process, drastically reduced the AIV replication in CLEC213 cells, without apparent cellular toxicity. Collectively, our results suggest that AIV is able to boost the metabolic capacities of its avian host in order to provide the important energy needs required to produce progeny virus.

| S-EPMC5404788 | biostudies-literature

mRNA and miRNA analysis during hepatitis C virus infection

Project description:This SuperSeries is composed of the SubSeries listed below.

2013-02-17 | GSE44370 | GEO

Macrophage-epithelial paracrine crosstalk inhibits lung edema clearance during influenza infection.

Project description:Influenza A viruses (IAV) can cause lung injury and acute respiratory distress syndrome (ARDS), which is characterized by accumulation of excessive fluid (edema) in the alveolar airspaces and leads to hypoxemia and death if not corrected. Clearance of excess edema fluid is driven mostly by the alveolar epithelial Na,K-ATPase and is crucial for survival of patients with ARDS. We therefore investigated whether IAV infection alters Na,K-ATPase expression and function in alveolar epithelial cells (AECs) and the ability of the lung to clear edema. IAV infection reduced Na,K-ATPase in the plasma membrane of human and murine AECs and in distal lung epithelium of infected mice. Moreover, induced Na,K-ATPase improved alveolar fluid clearance (AFC) in IAV-infected mice. We identified a paracrine cell communication network between infected and noninfected AECs and alveolar macrophages that leads to decreased alveolar epithelial Na,K-ATPase function and plasma membrane abundance and inhibition of AFC. We determined that the IAV-induced reduction of Na,K-ATPase is mediated by a host signaling pathway that involves epithelial type I IFN and an IFN-dependent elevation of macrophage TNF-related apoptosis-inducing ligand (TRAIL). Our data reveal that interruption of this cellular crosstalk improves edema resolution, which is of biologic and clinical importance to patients with IAV-induced lung injury.

| S-EPMC4811131 | biostudies-literature

Interferons disrupt lung epithelial repair during recovery from respiratory infection

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-06-12 | GSE148712 | GEO