DescriptionThis thesis aims to understand the dynamic impact of injury on liver metabolism and protein production. Hypermetabolism is a major clinical complication arising from systemic inflammation in the liver. Thus, this thesis hypothesizes that major inflammation driving stressors will be able to induce both metabolic and pro-inflammatory changes to liver gene expression. Animals were induced into an inflammatory state either by Burn, Cecal Ligation and Puncture (CLP), or Sham Cecal Ligation and Puncture (SCLP). CLP and SCLP, characterized previously by their cytokine outputs, were functionally annotated and subjected to pathway analysis following RNA expression measurement. Acute phase differences between CLP and SCLP show a much more severe acute CLP response, including a significant number of anti-bacterial proteins. Long term responses to CLP compared to SCLP show a significant anti-inflammatory surge, along with signs of oxidative stress sensitivity. When primed with burn injury, the CLP acute inflammatory response becomes depressed, but surges back stronger at later time points, suggesting early immune vulnerability followed by deleterious overcompensation. Overall, these studies reveal an underlying complexity to the sepsis models that suggest multiple avenues towards deleterious inflammation that may be clinically addressed.