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Expression data from mouse lungs during E. coli pneumonia in the presence or absence of LIF neutralization

ABSTRACT: Leukemia inhibitory factor (LIF) is amongst the IL-6 family cytokines expressed in the lungs during pneumonia. However, the function of endogenous LIF during pneumonia has never been explored. The purpose of this study was to determine the transcriptional response to pneumonia in the lungs and whether or how this response is influenced by LIF. Mice received intratracheal instillations of vehicle (PBS) or Escherichia coli (10^6 CFU). Control IgG or anti-LIF specific IgG was included in the instillate. 24 hours after the challenge, lungs were collected for RNA isolation and microarray analysis. RNA from 3 separate groups of mice (3 mice per group) was analyzed: 1) 24h Vehicle/control IgG-treated; 2) 24h E. coli/control IgG-treated; and 3) 24h E. coli/anti-LIF-specific IgG.

ORGANISM(S): Mus musculus

SUBMITTER: Lee Quinton

PROVIDER: E-GEOD-34901 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression data from mouse lungs during E. coli pneumonia in the presence or absence of LIF neutralization

Project description:Leukemia inhibitory factor (LIF) is amongst the IL-6 family cytokines expressed in the lungs during pneumonia. However, the function of endogenous LIF during pneumonia has never been explored. The purpose of this study was to determine the transcriptional response to pneumonia in the lungs and whether or how this response is influenced by LIF. Mice received intratracheal instillations of vehicle (PBS) or Escherichia coli (10^6 CFU). Control IgG or anti-LIF specific IgG was included in the instillate. 24 hours after the challenge, lungs were collected for RNA isolation and microarray analysis.

2012-04-26 | GSE34901 | GEO

Expression data from mouse lung epithelial cells during E. coli pneumonia in the presence or absence of LIF neutralization (6 h)

Project description:Leukemia inhibitory factor (LIF) is a cytoprotective cytokine that reduces lung injury during pneumonia. The purpose of this study was to determine the influence of LIF on pneumonia-induced gene changes in lung epithelium. Mice received intratracheal instillations of vehicle (PBS) or Escherichia coli (10^6 CFU). Control IgG or anti-LIF specific IgG was included in the instillate. 6 hours after the challenge, lung epithelial cells (EpCAM+/CD45-) were sorted from enzymatic lung digests and used for RNA isolation and microarray analysis.

2022-02-17 | GSE179419 | GEO

Expression data from mouse lung epithelial cells during E. coli pneumonia in the presence or absence of LIF neutralization (24 h)

Project description:Leukemia inhibitory factor (LIF) is a cytoprotective cytokine that reduces lung injury during pneumonia. The purpose of this study was to determine the influence of LIF on pneumonia-induced gene changes in lung epithelium. Mice received intratracheal instillations of vehicle (PBS) or Escherichia coli (10^6 CFU). Control IgG or anti-LIF specific IgG was included in the instillate. 24 hours after the challenge, lung epithelial cells (EpCAM+/CD45-) were sorted from enzymatic lung digests and used for RNA isolation and microarray analysis.

2022-02-17 | GSE179418 | GEO

Expression data from mouse livers expressing or lacking Cre recombinase during pneumonia

Project description:Cre-recombinase expression under control of an albumin promoter in the presence of floxed alleles is a highly effective and specific way to target gene mutations in hepatocytes. However, some concerns have been raised regarding off-target and/or toxic effects of cre itself, possibly confounding the interpretation of studies employing this approach. We have now used this tool to succesfully target gene deletions in hepatocytes during pneumonia, a condition which results in significant remodeling of the hepatic transcriptome. The goal of this study was to determine what effects, if any, cre expression alone has on hepatic gene expression during bacterial pneumonia. Mutant mice expressed CRE-recombinase under control of an albumin promoter. Results from mutants were compared to wild-type mice on the same genetic background (C57BL/6). Microarray analysis was performed on liver RNA collected from both genotypes of mice in the absence and presence of pneumococcal pneumonia. RNA from 2 separate groups of mice (3 mice per group) was analyzed: 1) Control mice infected intratracheally for 24h with 10^6 CFU of Streptococcus pneumoniae (serotype 3); and 2) Mutant mice infected intratracheally for 24h with 10^6 CFU of Streptococcus pneumoniae (serotype 3).

2012-02-16 | E-GEOD-35515 | biostudies-arrayexpress

Expression data from mouse livers lacking STAT3 during pneumonia

Project description:A common response to physiological duress is the hepatic acute phase response, a process during which the expression of many genes is altered in the liver. Amongst these transcripts are those encoding acute phase proteins, defined as circulating proteins with significantly changed concentrations during an acute phase response. The goal of this study was to determine the influence of STAT3 on hepatic gene changes including but not limited to acute phase proteins during bacterial pneumonia. Using the Cre-LoxP system, mice were generated with functional deletion of STAT3 in hepatocytes. In mutant mice, Cre-recombinase was expressed under transcriptional control of an albumin promoter in the presence of homozygous floxed alleles for STAT3. Wild-type control mice lacked the Cre-recombinase transgene. Microarray analysis was performed on liver RNA collected from both genotypes of mice in the absence and presence of pneumococcal pneumonia. RNA from 2 separate groups of mice (3 mice per group) was analyzed: 1) Control mice infected intratracheally for 24h with 10^6 CFU of Streptococcus pneumoniae (serotype 3); and 2) Mutant mice infected intratracheally for 24h with 10^6 CFU of Streptococcus pneumoniae (serotype 3).

2012-02-16 | E-GEOD-35514 | biostudies-arrayexpress

Expression data from mouse livers lacking NF-kappaB RelA (p65) during pneumonia

Project description:A common response to physiological duress is the hepatic acute phase response, a process during which the expression of many genes is altered in the liver. Amongst these transcripts are those encoding acute phase proteins, defined as circulating proteins with significantly changed concentrations during an acute phase response. The goal of this study was to determine the influence of NF-kappaB RelA (p65) on hepatic gene changes including but not limited to acute phase proteins during bacterial pneumonia. Using the Cre-LoxP system, mice were generated with functional deletion of NF-kappaB RelA (p65) in hepatocytes. In mutant mice, Cre-recombinase was expressed under transcriptional control of an albumin promoter in the presence of homozygous floxed alleles for RelA. Wild-type control mice lacked the Cre-recombinase transgene. Microarray analysis was performed on liver RNA collected from both genotypes of mice in the absence and presence of pneumococcal pneumonia. RNA from 2 separate groups of mice (3 mice per group) was analyzed: 1) Control mice infected intratracheally for 24h with 10^6 CFU of Streptococcus pneumoniae (serotype 3); and 2) Mutant mice infected intratracheally for 24h with 10^6 CFU of Streptococcus pneumoniae (serotype 3).

2012-02-16 | E-GEOD-35513 | biostudies-arrayexpress

Expression data from mouse livers lacking STAT3 and RelA during pneumonia

Project description:A common response to physiological duress is the hepatic acute phase response, a process during which the expression of many genes is altered in the liver. Amongst these transcripts are those encoding acute phase proteins, defined as circulating proteins with significantly changed concentrations during an acute phase response. The goal of this study was to determine the influence of two transcription factors, STAT3 and NF-kappaB p65 (RelA), on hepatic gene changes including but not limited to acute phase proteins during bacterial pneumonia. Using the Cre-LoxP system, mice were generated with combined functional deletions of both STAT3 and RelA in hepatocytes. In mutant mice, Cre-recombinase was expressed under transcriptional control of an albumin promoter in the presence of homozygous floxed alleles for both STAT3 and RelA. Wild-type control mice lacked the Cre-recombinase transgene. Microarray analysis was performed on liver RNA collected from both genotypes of mice in the absence and presence of pneumococcal pneumonia. RNA from 4 separate groups of mice (3 mice per group) was analyzed: 1) Uninfected wild-type control mice; 2) Uninfected mutant mice lacking liver STAT3 and RelA; 3) Control mice infected intratracheally for 24h with 10^6 CFU of Streptococcus pneumoniae (serotype 3); and 4) Mutant mice infected intratracheally for 24h with 10^6 CFU of Streptococcus pneumoniae (serotype 3).

2012-02-16 | E-GEOD-32105 | biostudies-arrayexpress

Mouse livers during pneumonia

Project description:This SuperSeries is composed of the following subset Series: GSE32105: Expression data from mouse livers lacking STAT3 and RelA during pneumonia GSE35513: Expression data from mouse livers lacking NF-kappaB RelA (p65) during pneumonia GSE35514: Expression data from mouse livers lacking STAT3 during pneumonia GSE35515: Expression data from mouse livers expressing or lacking Cre recombinase during pneumonia Refer to individual Series

2012-02-16 | E-GEOD-35516 | biostudies-arrayexpress

Oncostatin M neutralization in E. coli pneumonia

Project description:Oncostatin M (OSM) is an IL-6 family cytokine that is necessary for neutrophil recruitment in pneumonia by inducing STAT3-dependent production of CXCL5. We used microarrays to identify additional pathways affected by OSM neutralization in the lungs during pneumonia.

2021-03-08 | GSE155283 | GEO

Neutrophil depletion experiment in ischemia reperfusion mouse model

Project description:To elucidate the role of neutrophils in the molecular alterations observed after I/R, we performed an experiment of I/R in neutrophil-depleted mice. Neutrophil depletion was performed by anti-Ly6G injection and IgG was used as vehicle. We have performed an unbiased, open-search analysis of the oxidative PTMs and quantitative multiplexed proteomics that take place in the mouse heart tissue at 24h after I/R. Neutrophil depletion was performed in 3 mice by Ly6G injection 24h and 48 h prior to I/R and sacrificed 24 hours after reperfusion. A second group consisting on 3 mice that were injected with IgG antibody as vehicle, and subjected to I/R and sacrificed 24h after reperfusion. A third group of 3 mice with no injection were also sacrificed 24h after reperfusion. 12 additional mice from the three previous groups were sacrificed without I/R intervention: control without injection (n=6), IgG injection (n=3) and Ly6G injection (n=3). Whole hearts tissue was collected for proteomics evaluation.

2024-05-24 | PXD045756 | Pride

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