ABSTRACT: 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.
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-κB RelA or not.
Project description:A murine model of RelA mutated throughout the alveolar epithelium was generated. Mice were anesthetized and intratracheally instilled with 50M-NM-<g LPS into the left lung lobe. Mice were euthanized after 6 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 LPS stimulation 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.
Project description:PCR array of inflammatory cytokines and receptors in mouse lungs with NF-kappaB RelA mutant in alveolar epithelial cells during LPS stimulation
Project description:A murine model of RelA mutated throughout the alveolar epithelium was generated. Mice were anesthetized and intratracheally instilled with 50μg LPS into the left lung lobe. Mice were euthanized after 6 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 LPS stimulation are dependent on alveolar epithelial NF-κB RelA or not.
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.
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).
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
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.
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).