Pro- and anti-inflammatory cytokines operate as highly complex network systems featuring synergism, antagonism and functional redundancy whose deregulations feature prominently in the systemic inflammation vyhich characterises sepsis. Most studies conducted to date have focussed on single or small groups of cytokines as biomarkers of sepsis with mixed results, possibly due to a lack of recognition of their effects as a network output rather than as individual mediators. Severe sepsis has also proven to be a difficult condition to manage because of a lack of available therapeutic interventions to control its wayward inflammation. In this respect, simvastatin has recently been shown to alter cytokines in a number of different models of sepsis, making this an attractive candidate warranting fuller investigation. This study therefore aimed (i) to investigate a larger panel of cytokines (including some novel mediators) in order to assess their role(s) in the pathophysiology of sepsis and the mechanism(s) governing the regulation of their production, and (ii) to assess the purported anti-inflammatory effects of simvastatin on cytokine production.