Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-Seq analysis of skeletal muscles of mice with chronic or acute infections of LCMV Armstrong and LCMV clone 13

ABSTRACT: Chronic but not acute infections cause cachexia, characterized by bodyweight reduction and muscle loss. The underlying mechanisms remain incompletely understood. It is also not clear if muscle, in turn, regulates antiviral immune responses. In this study, we use two infection mouse models, one is acute and the other is chronic (described in PMID6332167 and PMID17950003), to study the global transcript profiles in muscles during infections.

ORGANISM(S): Mus musculus

PROVIDER: GSE134928 | GEO | 2020/04/08

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Longitudinal expression data from CD4+ T cells responding to LCMV-Armstrong or LCMV-Clone 13

Project description:During acute viral infections, naïve CD4+ T cells differentiate into effector CD4+ T cells and, after viral control, into memory CD4+ T cells. Memory CD4+ T cells are highly functional, proliferate rapidly upon reinfection and persist long-term without antigen. In contrast, during chronic infections, CD4+ T cells become less functional. To compare the development of functional memory T cells with poorly functional T cells from chronic viral infection, we generated longitudinal transcriptional profiles for each. Naive CD44Lo CD4+ T cells were isolated and sorted from uninfected C57BL/6 mice and H2-IAb GP66-specific CD4+ T cells were sorted using MHC-II tetramers at d6, 8, 15, and 30 p.i. with either LCMV Arm or LCMV clone 13. RNA from these CD4+ T cells was processed, amplified, labeled, and hybridized to Affymetrix GeneChip MoGene 1.0 st microarrays.

2014-10-24 | E-GEOD-41866 | biostudies-arrayexpress

Longitudinal expression data from CD4+ T cells responding to LCMV-Armstrong or LCMV-Clone 13

2014-10-24 | GSE41866 | GEO

Longitudinal expression data from CD8+ T cells responding to LCMV-Armstrong or LCMV-Clone 13

Project description:During acute viral infections, naïve CD8+ T cells differentiate into effector CD8+ T cells and, after viral control, into memory CD8+ T cells. Memory CD8+ T cells are highly functional, proliferate rapidly upon reinfection and persist long-term without antigen. In contrast, during chronic infections, CD8+ T cells become “exhausted” and have poor effector function, express multiple inhibitory receptors, possess low proliferative capacity, and cannot persist without antigen. To compare the development of functional memory T cells with poorly functional exhausted T cells, we generated longitudinal transcriptional profiles for each. Naive CD44Lo CD8+ T cells were isolated and sorted from uninfected C57BL/6 mice and H2-Db GP33-specific CD8+ T cells were sorted using MHC-I tetramers at d6, 8, 15, and 30 p.i. with either LCMV Arm or LCMV clone 13. RNA from these CD8+ T cells was processed, amplified, labeled, and hybridized to Affymetrix GeneChip MoGene 1.0 st microarrays

2012-11-23 | E-GEOD-41867 | biostudies-arrayexpress

Longitudinal expression data from CD8+ T cells responding to LCMV-Armstrong or LCMV-Clone 13

2012-11-23 | GSE41867 | GEO

RNA-Seq analysis of skeletal muscles of mice with chronic or acute infections of LCMV Armstrong and LCMV clone 13

Project description:RNA-Seq analysis of skeletal muscles of mice with chronic or acute infections of LCMV Armstrong and LCMV clone 13

| PRJNA556820 | ENA

Comparison of monocytic cells from naïve mice and day 14 LCMV Armstrong and day 14 LCMV Clone 13 infected mice

Project description:Infection with acute and chronic strains of LCMV (Armstrong (ARM) and Clone 13 (C13), respectively) leads to massive proliferation of monocytic cells contemporaneously with peak of the anti-viral CD8+ T cell response. These cells return to naïve levels following ARM infection. However, during C13 infection these cells are sustained at high levels and gain a T cell suppressive function at day 14 post infection. The mechanisms by which these cells are induced to proliferate and impair T cell function during chronic LCMV infection are largely unknown. To address this, we analyzed gene expression profiles using microarray analysis of purified splenic monocytic cells (CD11b+ Ly6Chi Gr-1low) from naïve mice, or day 14 LCMV ARM or LCMV C13 infected mice.

2013-02-25 | GSE43896 | GEO

Expression profiling of muscles in NOD-SCID mice bearing RXF and SKR tumors

Project description:Cachexia is a devastating muscle wasting syndrome that occurs in patients suffering from chronic diseases, most commonly observed in 80% of advanced cancer patients. One of the primary causes of cachexia-associated morbidity and mortality is involuntary muscle wasting. And while many cachexia patients show hypermetabolism, its causative role in muscles had remained unclear. To understand the molecular basis of this muscle wasting, accurate models of cachexia are necessary. Using transcriptomics and cytokine profiling of human muscle stem cell-based models and human cancer-induced cachexia models in mice, we found that cachectic cancer cells secreted many inflammatory factors which rapidly led to higher levels of fatty acid metabolism and the activation of a p38 stress response signature, before the cachectic muscle wasting is manifested. Metabolomics profiling revealed that factors secreted by cachectic cancer cells rapidly induce excessive fatty acid oxidation in human myotubes, leading to oxidative stress, p38 activation, and impaired muscle growth. Pharmacological blockade of fatty acid oxidation not only rescued human myotubes, but also significantly improved muscle mass and total weight in cancer cachexia models in vivo. Therefore, fatty acid-induced oxidative stress could be targeted to prevent cancer cachexia.

2016-05-01 | GSE80081 | GEO

CD4+ and CD8+ T cells responding to LCMV-Armstrong or LCMV-Clone 13

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

2012-12-19 | E-GEOD-41870 | biostudies-arrayexpress

CD4+ and CD8+ T cells responding to LCMV-Armstrong or LCMV-Clone 13

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

2012-12-19 | GSE41870 | GEO

Primary and secondary CD8 T cells during acute and chronic LCMV infection

Project description:Understanding the response of memory CD8 T cells to persistent antigen re-stimulation and the role of CD4 T cell help is critical to the design of successful vaccines for chronic diseases. However, studies comparing the protective abilities and qualities of memory and naïve cells have been mostly performed in acute infections, and little is known about their roles during chronic infections. Herein, we show that memory cells dominate over naïve cells and are protective when present in large enough numbers to quickly reduce infection. In contrast, when infection is not rapidly reduced, memory cells are quickly lost, unlike naïve cells. This loss of memory cells is due to (i) an early block in cell proliferation, (ii) selective regulation by the inhibitory receptor 2B4, and (iii) increased reliance on CD4 T cell help. These findings have important implications towards the design of T cell vaccines against chronic infections and tumors. 16 samples are analyzed: 3 replicates of secondary effector CD8 P14 T cells at day 8 post-acute lymphocytic choriomeningitis virus (LCMV) infection; 4 replicates of secondary effector CD8 P14 T cells at day 8 post-chronic LCMV infection; 4 replicates of primary effector CD8 P14 T cells at day 8 post-acute LCMV infection; and 5 replicates of primary effector CD8 P14 T cells at day 8 post-chronic LCMV infection.

2011-08-22 | E-GEOD-30962 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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