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Prior elevation of IL‐18 promotes rapid early IFN‐γ production during staphylococcal infection

Systemic Staphylococcus aureus infection is associated with significant morbidity and mortality arising from both bacterial and host immune factors. IL‐18 is a pro‐inflammatory cytokine of the IL‐1 superfamily that exhibits broad functional effects in innate and acquired immune responses and which has been found in high levels in several chronic inflammatory and autoimmune diseases. Over‐expression of IL‐18 may promote early resolution of infection or could promote a detrimental exaggerated immune response. This was explored in a model of S. aureus infection. We report increased mortality in Swiss mice that were given recombinant IL‐18 prior to inoculation with S. aureus LS‐1. IL‐18 administration prior to infection induced preferentially enhanced IFN‐γ mRNA expression in peripheral blood leukocytes and spleen, especially splenic NK cells. This correlated with increased IFN‐γ protein detection in serum, and leukocyte and spleen cultures at subsequent discrete time points. These data suggest that increased mortality following gram‐positive infection in autoimmune diseases could in part reflect the impact of high levels of pleiotropic pro‐inflammatory cytokines such as IL‐18 present prior to the onset of infection.