Mus musculus
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ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-3203
PROVIDER: PRJNA92871 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Transcription profiling of mouse influenza virus infected in wild type and mutant animals revels induced gene expression changes of regional B cells are mediated in part through type I IFN
2014-10-10 | E-GEOD-3203 | ExpressionAtlas
Project description:Influenza virus infection-induced gene expression changes of regional B cells are mediated at least in part through type I Interferon: Our objective is to determine whether the influenza virus-infection induced gene expression changes in regional lymph node B cells are facilitated at least in part through type I interferon. Our specific aim is to compare the gene expression profile of highly FACS-purified B cells in the regional lymph nodes of wildtype and IFNR-/- mice prior to and 48h following infection with influenza virus infection and to contrast this expression profile with that of FACS-purified wildtype B cells activated in vitro with IFN-beta +/- anti-CD86 for 12h. Keywords: Infection-induced responses
2006-08-26 | GSE3203 | GEO
Project description:Influenza virus infection-induced gene expression changes of regional B cells are mediated at least in part through type I Interferon:; Our objective is to determine whether the influenza virus-infection induced gene expression changes in regional lymph node B cells are facilitated at least in part through type I interferon. Our specific aim is to compare the gene expression profile of highly FACS-purified B cells in the regional lymph nodes of wildtype and IFNR-/- mice prior to and 48h following infection with influenza virus infection and to contrast this expression profile with that of FACS-purified wildtype B cells activated in vitro with IFN-beta anti-CD86 for 12h. Experiment Overall Design: We analyzed gene expression from mouse lymph node B cells purified by flow cytometric sorting using single channel oligonucleotide microarrays. There were 4 groups: 1) wild type uninfected mice (control group), 2) wild type mice infected with influenza (flu) for 2 days, 3) IFNR-/- mice infected with flu for 2 days, 4) cells stimulated with IFN-b in vitro for 17 h. Each group contained 4 biological replicates obtained from independent experiments. There were 16 total samples and each was measured on a separate array.
2010-08-04 | E-GEOD-3203 | biostudies-arrayexpress
Project description:Type I interferon (IFN) is the first line of defense against virus infection. By using both in vivo and in vitro influenza infection models, we found that type I IFN-κ, limited the replication of influenza viruses by stimulating a IFNAR-MAPK-cFos-CHD6 axis. Similarly, Zika virus (ZIKV) was also highly sensitive to IFN-κ-mediated suppression. With an IAV infected mouse model, we found that IFN-κ was the earliest responding type I interferon among all known members in mice after H9N2 infection, a low-pathogenic Avian Influenza, whereas this early induction did not occur upon highly pathogenic H7N9 infection. IFN-κ can efficiently contain both low- and high-pathogenic influenza replication in cultured human lung cells, and CHD6 was the major effector responsive molecule for IFN-κ, but not for IFN-α/β. Furthermore, we discovered that both IFNAR1 and IFNAR2 subunits of type I interferon receptor and their downstream axis of p38-cFos are engaged in IFN-κ signaling cascade to acti vate CHD6, which didn`t require STAT1 activity. In addition, we showed that the pre-treatment with IFN-κ before IAV challenge protected mice from high mortality. Altogether, our study identified an IFN-κ-specific pathway that suppressed influenza A virus in vitro and in vivo. Thus, IFN-κ may have potential as a new prevention and treatment agents against emerging viruses
2020-04-09 | GSE142708 | GEO
Project description:Type I interferon (IFN) is the first line of defense against virus infection. By using both in vivo and in vitro influenza infection models, we found that type I IFN-κ, limited the replication of influenza viruses by stimulating a IFNAR-MAPK-cFos-CHD6 axis. Similarly, Zika virus (ZIKV) was also highly sensitive to IFN-κ-mediated suppression. With an IAV infected mouse model, we found that IFN-κ was the earliest responding type I interferon among all known members in mice after H9N2 infection, a low-pathogenic Avian Influenza, whereas this early induction did not occur upon highly pathogenic H7N9 infection. IFN-κ can efficiently contain both low- and high-pathogenic influenza replication in cultured human lung cells, and CHD6 was the major effector responsive molecule for IFN-κ, but not for IFN-α/β. Furthermore, we discovered that both IFNAR1 and IFNAR2 subunits of type I interferon receptor and their downstream axis of p38-cFos are engaged in IFN-κ signaling cascade to acti vate CHD6, which didn`t require STAT1 activity. In addition, we showed that the pre-treatment with IFN-κ before IAV challenge protected mice from high mortality. Altogether, our study identified an IFN-κ-specific pathway that suppressed influenza A virus in vitro and in vivo. Thus, IFN-κ may have potential as a new prevention and treatment agents against emerging viruses
2020-04-09 | GSE142707 | GEO
Project description:Transcription profiling by array of HUVEC cells after infection with H5N1 influenza virus
2025-01-24 | E-GEOD-13637 | ExpressionAtlas
Project description:ICL010 - Infection of Calu-3 cells with H1N1 influenza virus A/Netherlands/602/2009
2025-01-24 | E-GEOD-40844 | ExpressionAtlas
Project description:CD8+ cytotoxic T cells are critical for viral clearance from the lungs upon influenza virus infection. The contribution of cross-presentation to the induction of anti-viral cytotoxic T cells remains debated. Here, we used a recombinant influenza virus expressing a NS1-GFP reporter gene to visualize the route of antigen presentation by lung dendritic cells (DC) upon viral infection in vivo. We found that lung CD103+ DC are the only subset to carry intact GFP protein to the draining lymph nodes. Strikingly, lung migratory CD103+ DC are not productively infected by influenza virus and thus induce virus-specific CD8+ T cells through the cross-presentation of antigens from virally infected cells. We also show that CD103+ DC resistance to infection correlates with an increased antiviral state in these cells that is dependent on the expression of IFN receptor alpha. In conclusion, these results establish that efficient cross-priming by migratory lung DC is coupled to the acquisition of an anti-viral status, which is dependent on type I IFN signaling pathway. mRNA profiles were generated by deep-sequencing in Illumina HiSeq2000 from alveolar macrophages and CD103+ dendritic cells from lungs of untreated and flu-treated mice
2013-06-19 | E-GEOD-38838 | biostudies-arrayexpress
Project description:A. Esteban Hernandez-Vargas & Michael Meyer-Hermann. Innate Immune System Dynamics to Influenza Virus. IFAC Proceedings Volumes 45, 18 (2012).
The understanding of how influenza virus infection activates the immune system is crucial to designing prophylactic and therapeutic strategies against the infection. Nevertheless, the immune response to influenza virus infection is complex and remains largely unknown. In this paper we focus in the innate immune response to influenza virus using a mathematical model, based on interferon-induced resistance to infection of respiratory epithelial cells and the clearance of infected cells by natural killers. Simulation results show the importance of IFN-I to prevent new infections in epithelial cells and to stop the viral explosion during the first two days after infection. Nevertheless, natural killers response might be the most relevant for the first depletion in viral load due to the elimination of infected cells. Based on the reproductive number, the innate immune response is important to control the infection, although it would not be enough to clear completely the virus. The effective coordination between innate and adaptive immune response is essential for the virus eradication.
2024-09-02 | BIOMD0000000710 | BioModels
Project description:Influenza defective interfering (DI) viruses have long been considered promising antiviral candidates because of their ability to interfere with replication-competent viruses and to induce antiviral immunity. However, the mechanisms underlying DI-mediated antiviral immunity have not been extensively explored. Here, we demonstrated interferon (IFN) independent protection conferred by influenza DI virus against homologous virus infection in mice deficient in type I and III IFN signaling. By integrating transcriptional and post-transcriptional regulatory data we identified unique host signatures in response to DI co-infection. DI-treated mice exhibited reduced viral transcription, less intense inflammatory and innate immune responses, and primed multiciliated cell differentiation in their lungs at an early stage of infection, even in the absence of type I or III IFNs. This increased multiciliogenesis could also be detected at the protein level by immunofluorescence staining of lung tissue from DI-treated mice. Overall, our study provides mechanistic insight into the protection mediated by DIs, implying a unifying theme involving inflammation and multiciliogenesis in maintaining respiratory homeostasis, and reveals their IFN-independent antiviral activity.
2023-05-15 | GSE188122 | GEO