Mouse livers lacking NF-kappaB RelA (p65) during bacteremia

Using a mouse model with hepatocyte-specific deletion of transcription factor NF-κB RelA (p65), our group has previously revealed the important role of RelA in inducing the acute phase response, maintaining host defense, and preventing liver injury during sepsis. To goal of this study was determine the influence of RelA on hepatic gene changes that provide liver protection during infection. Mice were generated with functional deletion of NF-kappaB RelA (p56) in hepatocytes using a Cre-LoxP system. Mutant mice expressed Cre-recombinase under the transcriptional control of an albumin promotor and homozygous floxed RelA alleles. Wild type control mice lack the Cre-recombinase. Microarray analysis was performed on liver RNA collected from both genotypes of mice in the absence and presence of pneumococcal bacteremia. RNA samples from liver tissue of control or mutant mice infected intravenously with 10^6 CFU of Streptococcus pneumoniae (serotype 3) at three time points (0, 6, and 24 hours) were analyzed. (n = 3 to 5 biological replicates per group)