Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

An ultrasensitive mechanism regulates influenza virus-induced inflammation

ABSTRACT: Whole-genome, time-course data was developed from the lungs of influenza infected mice to better characterize the dynamics of the host immune response during infection.

ORGANISM(S): Mus musculus

PROVIDER: GSE63786 | GEO | 2015/06/12

SECONDARY ACCESSION(S): PRJNA269067

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

An ultrasensitive mechanism regulates influenza virus-induced inflammation

Project description:Whole-genome, time-course data was developed from the lungs of influenza infected mice to better characterize the dynamics of the host immune response during infection. Lung for microarray studies were obtained from female, five-week old C57BL/6Js infected with influenza viruses. Forty-two animals per group were inoculated with 10^5 PFU of A/Kawasaki/UTK-4/09 H1N1 virus [Kawasaki], A/California/04/09 (H1N1) virus (pH1N1) [SOIV], A/Vietnam/1203/04 H5N1 virus (H5N1), 10^3 PFU A/Vietnam/1203/04 H5N1 virus (H5N1) [VN1203] or mock-infected with PBS. Spanning the first week of the infections, three animals per infection group were sacrificed at 14 predetermined time points, lungs isolated and the homogenate was used to assess changes in genes expression over time and between infections.

2015-06-12 | E-GEOD-63786 | biostudies-arrayexpress

An Ultrasensitive Mechanism Regulates Influenza Virus-Induced Inflammation.

Project description:Influenza viruses present major challenges to public health, evident by the 2009 influenza pandemic. Highly pathogenic influenza virus infections generally coincide with early, high levels of inflammatory cytokines that some studies have suggested may be regulated in a strain-dependent manner. However, a comprehensive characterization of the complex dynamics of the inflammatory response induced by virulent influenza strains is lacking. Here, we applied gene co-expression and nonlinear regression analysis to time-course, microarray data developed from influenza-infected mouse lung to create mathematical models of the host inflammatory response. We found that the dynamics of inflammation-associated gene expression are regulated by an ultrasensitive-like mechanism in which low levels of virus induce minimal gene expression but expression is strongly induced once a threshold virus titer is exceeded. Cytokine assays confirmed that the production of several key inflammatory cytokines, such as interleukin 6 and monocyte chemotactic protein 1, exhibit ultrasensitive behavior. A systematic exploration of the pathways regulating the inflammatory-associated gene response suggests that the molecular origins of this ultrasensitive response mechanism lie within the branch of the Toll-like receptor pathway that regulates STAT1 phosphorylation. This study provides the first evidence of an ultrasensitive mechanism regulating influenza virus-induced inflammation in whole lungs and provides insight into how different virus strains can induce distinct temporal inflammation response profiles. The approach developed here should facilitate the construction of gene regulatory models of other infectious diseases.

| S-EPMC4457877 | biostudies-literature

Lethal dissemination of H5N1 influenza virus is associated with dysregulation of inflammation and lipoxin signaling in a mouse model of infection

2013-07-16 | GSE48890 | GEO

Influenza A virus

Project description:Intra- and inter-host evolutionary dynamics of mammalian influenza viruses

| PRJNA255651 | ENA

FluOMICS - Metabolomics analysis of mouse lungs infected with H1N1 influenza virus

Project description:Metabolomics analysis of C57BL/6 mouse lungs infected with influenza A/California/04/09 (H1N1) virus, mock infected with PBS, or untreated.

2017-12-06 | MSV000081785 | MassIVE

scRNA-seq of young and aged lungs following influenza A virus infection

Project description:Aging is known to alter the host repsonse to influenza infection. Here, we use single-cell RNA sequencing (scRNA-seq) to identify cellular changes in the lungs of young (16-week-old) and aged (80-week-old) mice following influenza infection.

2023-09-05 | GSE202325 | GEO

Spatial sequencing of young and aged lungs following influenza A virus infection

Project description:Aging is known to alter the host repsonse to influenza infection. Here, we use 10x Visium spatial sequencing to identify spatial changes in mRNA expression of left lungs of young (16-week-old) and aged (80-week-old) mice following influenza infection.

2023-10-16 | GSE202322 | GEO

Bulk RNA-seq of young and aged lungs following influenza A virus infection

Project description:Aging is known to alter the host repsonse to influenza infection. Here, we use bulk RNA sequencing (bulk RNA-seq) to identify cellular changes in the lungs of young (16-week-old) and aged (80-week-old) mice following influenza infection.

2023-09-05 | GSE202324 | GEO

FluOMICS - Metabolomics analysis of mouse lungs infected with H5N1 (HALo) influenza virus

Project description:Metabolomics analysis of C57BL/6 mouse lungs infected with influenza A/Vietnam/1203/04 (H5N1) HALo virus, mock infected with PBS, or untreated.

2017-12-06 | MSV000081786 | MassIVE

Lethal dissemination of H5N1 influenza virus is associated with dysregulation of inflammation and lipoxin signaling in a mouse model of infection

Project description:Periodic outbreaks of highly pathogenic avian H5N1 influenza viruses and the current H1N1 pandemic highlight the need for a more detailed understanding of influenza virus pathogenesis. To investigate the host transcriptional response induced by pathogenic influenza viruses, we used a functional-genomics approach to compare gene expression profiles in lungs from wild-type 129S6/SvEv and interferon receptor (IFNR) knockout mice infected with either the fully reconstructed H1N1 1918 pandemic virus (1918) or the highly pathogenic avian H5N1 virus Vietnam/1203/04 (VN/1203). Eight- to 10-week-old female wild-type and IFNR1-/- mice (on a 129S6/SvEv background) were anesthetized by intraperitoneal injection of 0.2 ml of 2,2,2-tribromoethanol in tert-amylalcohol (Avertin; Sigma-Aldrich, Milwaukee, WI). Ten times the 50% lethal dose (LD50), 3.2 × 10^4 PFU (1918) or 7 × 10^3 PFU (VN/1203), in 50 μl of infectious virus diluted in phosphate-buffered saline (PBS) was inoculated intranasally (i.n.). Lung tissue was harvested for microarray analysis from infected animals at 1, 3, and 4 days post-innoculation. For RNA isolation, lungs were frozen in individual tubes and stored in solution D (4 M guanidinium thiocyanate, 25 mM sodium citrate, 0.5% sarcosyl, 0.1 M β-mercaptoethanol). Separate microarrays were run for each infected mouse. This included 2 animals/time point for 1918 virus-infected mice (24 animals total) or 3 animals/time point for VN/1203-infected mice (36 animals total). Lung tissue from three uninfected wild type 129S6/SvEv mice was collected as a mock control. Equal masses of total RNA from the lung tissue of the three mice were pooled prior to being run on microarray. Two-channel microarrays were used to determine gene expression in the lungs. For each individual infected lung, gene expression from an infected lung was compared to gene expression from the pooled RNA from the mock control.

2013-07-16 | E-GEOD-48890 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data