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Expression data from mouse livers lacking STAT3 during pneumonia

ABSTRACT: 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).

ORGANISM(S): Mus musculus

SUBMITTER: Lee Quinton

PROVIDER: E-GEOD-35514 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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

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 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

2012-02-16 | GSE35514 | GEO

Expression data from mouse livers lacking STAT3 and RelA during pneumonia

2012-02-16 | GSE32105 | GEO

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

2012-02-16 | GSE35513 | GEO

PCR array of inflammatory cytokines and receptors in mouse lungs with NF-kappaB RelA mutant in alveolar epithelial cells during pneumococcal pneumonia

2012-08-03 | GSE38399 | GEO

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

PCR array of inflammatory cytokines and receptors in mouse lungs with NF-kappaB RelA mutant in alveolar epithelial cells during pneumococcal pneumonia

Project description:A murine model of RelA mutated throughout the alveolar epithelium was generated. Mice were anesthetized and intratracheally instilled with 106 CFU of Streptococcus pneumoniae serotype 3 into the left lung lobe. Mice were euthanized after 15 hours after instillation, and left lung lobes were collected to isolate RNA. We used SABioscience Mouse Inflammatory Cytokines and Receptors PCR Array to evaluate whether the expressions of lung cytokines and receptors during pneumococcal pneumonia are dependent on alveolar epithelial NF-M-NM-:B RelA or not. qPCR gene expression profiling. RNA were collected from six different mouse lungs in each genotype (wild-type and alveolar epithelial RelA mutant). Equal amount of RNA (200ng) was pooled from six different mouse lungs, and 1M-NM-<g of total RNA (1.2M-NM-<g) was used to the PCR array.

2012-08-03 | E-GEOD-38399 | biostudies-arrayexpress

Pneumonia infection, lung and liver inflammation

Project description:Vaccination reduces morbidity and mortality from pneumonia but its effect on the tissue-level response to infection is still poorly understood. We evaluated pneumonia disease progression, acute phase response and lung gene expression profiles in mice inoculated intranasally with virulent gram-positive Streptococcus pneumoniae serotype (ST) 3, with and without prior immunization with pneumococcal polysaccharide ST 3 (PPS3), or co-immunization with PPS3 and with a low dose of lipopolysaccharide (LPS). Pneumonia severity was assessed in the acute phase, 5, 12, 24 and 48 h post-inoculation (p.i.) and the resolution phase of 7 days p.i. Primary PPS3 specific antibody production was upregulated and IgM binding to pneumococci increased in PPS3-immunized mice. Immunizations with PPS3 or PPS3 + LPS decreased bacterial recovery the lung and blood at 24 and 48 h and increased survival. Microarray analysis of whole lung RNA revealed significant changes in the acute phase protein serum amyloid A (SAA) between noninfected and infected mice, which were attenuated by immunization. SAA transcripts were higher in the liver and lungs of infected controls, and SAA protein was elevated in serum, but decreased in PPS3-immunized mice. Thus, during a virulent pneumonia infection, prior immunization with PPS3 in an IgM-dependent manner as well as co-immunization with PPS3 + LPS attenuated pneumonia severity and promoted resolution of infection, concomitant with significant regulation of cytokine gene expression in the lungs, and acute phase proteins in the lungs, liver and serum.

2013-03-29 | GSE45644 | GEO

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