Our study has its limitations. To translate the present findings, we are currently working on a clinical model to assess the clinical significance of ketamine's anti-inflammatory effects in patients with bacterial sepsis. Although studies of the effect of ketamine on macrophage responses to purified bacterial components such as Gram-negative lipopolysaccharide (LPS) or Gram-positive lipoteichoic acid (LTA) are instructive [23, 24, 49] , we argue that characterization of the macrophage responses to whole organisms is more likely to provide clinical insights. Indeed, the pioneering experiments of Carswell and Old that identified TNF used whole bacteria as stimuli in macrophage sepsis simulation settings [49] , and we have previously demonstrated that macrophage responses to live, antibiotic-treated staphylococci serve as a powerful model system. Furthermore, the model examines the effect of ketamine only in the presence of antibiotics (either vancomycin or daptomycin). In practice, this is a common clinical scenario. Our data suggest that clinically achievable concentrations of both ketamine and daptomycin could potentially inhibit the excessive macrophage inflammatory response that is observed in patients with severe staphylococcal infections.