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Timecourse of Interferon-Gamma Treatment of Bone Marrow-Derived Macrophages (BMDMs)

ABSTRACT: The systematic temporal gene expression analysis of primary macrophages activated under immune (interferon-gamma (IFN-g)) and productive viral infection with murine cytomegalovirus (mCMV). The primary objective of the study is to define, in an unbiased manner, cause-and-effect relationships in the program of gene activation in this cellular system. The even spacing and time intervals (every 30 minutes) makes this study amenable to modelling of gene networks in the system.

ORGANISM(S): Mus musculus

PROVIDER: GSE42504 | GEO | 2015/07/10

SECONDARY ACCESSION(S): PRJNA194400

REPOSITORIES: GEO

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Timecourse of mCMV Infection of Bone Marrow-Derived Macrophages (BMDMs)

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Timecourse of mCMV Infection of Bone Marrow-Derived Macrophages (BMDMs)

Project description:The systematic temporal gene expression analysis of primary macrophages activated under immune (interferon-gamma) and productive viral infection with murine cytomegalovirus (mCMV). The primary objective of the study is to define, in an unbiased manner, cause-and-effect relationships in the program of gene activation in this cellular system. The even spacing and time intervals (every 30 minutes) makes this study amenable to modelling of gene networks in the system. A kinetic analysis of mCMV infection on the gene expression of murine (BALB/c) bone marrow-derived macrophages (BMDMs) over the first 12 hours, sampling every 30 minutes. Agilent mouse genome arrays were used to determine the differences in gene expression between mock and mCMV infected. The 25 samples collected for the mock infected were pooled and treated as a pooled control. Pooled control was labelled with Cy3 dye and hybridised with every other sample (labelled with Cy5 dye) = 25 dual-dye array hybridisations. The reference channel of the dual-channel hybridisations was only used to normalise the expression of the test channel, rather than used to calculate ratio data. Thus, the normalised data represent log2 single-channel data.

2015-07-10 | E-GEOD-42503 | biostudies-arrayexpress

Timecourse of Interferon-Gamma Treatment of Bone Marrow-Derived Macrophages (BMDMs)

Project description:The systematic temporal gene expression analysis of primary macrophages activated under immune (interferon-gamma (IFN-g)) and productive viral infection with murine cytomegalovirus (mCMV). The primary objective of the study is to define, in an unbiased manner, cause-and-effect relationships in the program of gene activation in this cellular system. The even spacing and time intervals (every 30 minutes) makes this study amenable to modelling of gene networks in the system. A kinetic analysis of IFN-g treatment on the gene expression of murine (BALB/c) bone marrow-derived macrophages (BMDMs) over the first 12 hours, sampling every 30 minutes. Agilent mouse genome arrays were used to determine the differences in gene expression between mock and IFN-g treated. The 25 samples collected for the mock IFN-g treatment were pooled and treated as a pooled control. Pooled control was labelled with Cy3 dye and hybridised with every other sample (labelled with Cy5 dye) = 25 dual-dye array hybridisations. The reference channel of the dual-channel hybridisations was only used to normalise the expression of the test channel, rather than used to calculate ratio data. Thus, the normalised data represent log2 single-channel data.

2015-07-10 | E-GEOD-42504 | biostudies-arrayexpress

MCMV infection of cultured mouse cells induces expression of miR-7a.

Project description:One goal of viral infection is to reprogram the host cell to optimize viral replication. As part of this process, viral miRNAs may compete for components of the miRNA/siRNA pathway as well as regulate cellular targets. Mouse Cytomegalovirus has been described to generate large numbers of viral miRNAs during lytic infection and was therefore used to analyze the impact of viral miRNAs on the host cell small RNA system as well as to check for sorting of viral small RNAs into specific Ago-proteins. Deep sequencing analysis of MCMV infected cells revealed that viral miRNAs represent only app. 13% of all detected miRNAs. All previously described MCMV miRNAs with the exception of miR-m88-1* were confirmed and for the MCMV miR-m01-1 hairpin an additional miRNA, designated miR-m01-1-3p, was found. Its presence was confirmed by qPCR and Northern Blot. Deep sequencing after RISC IP with antibodies specific for either Ago1 or Ago2 showed that all MCMV miRNAs are loaded into both RISC complexes. The ratio of MCMV to mouse miRNAs was not increased after immunoprecipitation of Ago-proteins. Viral miRNAs therefore do not overwhelm the host miRNA processing system nor are they preferentially incorporated into RISC. We found that 3 mouse miRNAs showed an altered expression due to MCMV infection. Down-regulation of miR-27a, as previously described, could be confirmed. In addition, miR-26a was down-regulated and an up-regulation of miR-7a dependent on viral protein expression could be observed. Examination of small RNA expression in uninfected vs. infected cells, immunoprecipitation + sequencing of Ago1 and Ago2 loaded small RNAs in infected cells

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Project description:Ly49G2+ NK cells mediate essential control of murine cytomegalovirus (MCMV) infection in mice which express the H-2Dk class I molecule. As a cognate ligand for specific Ly49G2 inhibitory receptor allotypes, H-2Dk also licenses Ly49G2+ NK cells in naïve and MCMV-infected mice. These findings suggest Ly49G2 may promote antiviral NK cell activities during MCMV infection. Indeed, in mice lacking the Ly49G2 receptor, MCMV resistance is fully abrogated. Additionally, NK cells expressing Ly49R, an NK cell associated activation receptor that also recognizes H-2Dk, have their function augmented by Ly49G2 and are required for MCMV resistance.

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Acute murine cytomegalovirus infection boosts cell-type specific response and lipid metabolism changes in infant mice liver

Project description:Human cytomegalovirus (HCMV) infection in infants cause severe diseases, such as neonatal hepatitis. However, the single-cell dimensional description of the immune cell alteration during the first virus exposure process in infants, remains poorly understood. The hepatocytes play an essential role in metabolic homeostasis and detoxification. The Concomitant Effects of CMV infection on liver lipid metabolism in infants are still unclear. Here, using single-cell RNA-sequencing, we found MCMV can infect most cell types of infant mice liver, changing the number of immune cells. MCMV infection increases proliferating CD8 effector T cells and a subset of Nos2+ monocytes, which may play important roles in the early anti-viral process. Furthermore, MCMV infection subvert the protein expression profile of lipid metabolism in hepatocytes. Overall, our data provide insights as to how the immune system response to MCMV infection during the early stage of infection, and the impact of infection on lipid metabolism in infant mice hepatocytes.

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Natural killer cell sensing of infected cells compensates deficient Toll-like receptor but not IFN-I activity for mouse resistance to cytomegalovirus

Project description:Plasmacytoid dendritic cells (pDC) are the major source of type I IFN (IFN-I) in vivo during Murine Cytomegalovirus (MCMV) infection. This response requires pDC-intrinsic MyD88-dependent signaling by Toll Like Receptors 7/9. Provided that they express appropriate recognition receptors such as Ly49H, Natural Killer (NK) cells can directly sense and kill MCMV-infected cells. While MyD88- and Ly49H-dependent responses can contribute to MCMV control, the objective is to understand the relative importance of these 3 mechanisms. In order to decipher the relative impact of MyD88- and Ly49H-dependent mechanisms during MCMV infection, we performed a genome-wide expression analysis on total spleen of Ly49H-/-MyD88+/+, Ly49H-/-MyD88-/-, Ly49H+/+MyD88+/+ and Ly49H+/+MyD88-/- BALB/c mice at different time points after MCMV infection (d0, d1,5, d2, d3 and d6). This study includes data from the spleen BALB/c mice, under steady-state or MCMV condition at different time points. 2 to 5 mice for each mouse strain for each time point were used, and were hybridized on 5 separate batches of gene chips.

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