The role of interferon-γ in the pathogenesis of acute intra-abdominal sepsis

IFNγ produced by intraperitoneal myeloid and NK cells during cecal ligation/puncture‐induced septic shock facilitates myeloid cell activation yet blockade of IFNγ does not improve survival. Several studies indicate that IFN‐γ facilitates systemic inflammation during endotoxin‐induced shock. However, the pathobiology of IFN‐γ in clinically relevant models of septic shock, such as CLP, is not well understood. In this study, the role of IFN‐γ in the pathogenesis of CLP‐induced septic shock was evaluated by examining IFN‐γ production at the tissue and cellular levels. The impact of IFN‐γ neutralization on systemic inflammation, bacterial clearance, and survival was also determined. Following CLP, concentrations of IFN‐γ in plasma and peritoneal lavage fluid were low in comparison with concentrations of IL‐6 and MIP‐2, as was IFN‐γ mRNA expression in liver and spleen. The overall percentage of IFN‐γ+ splenocytes was