Introduction/Aims: The major complication of acute pancreatitis (AP) is secondary infection. We have previously observed in experimental AP, that the translocation of intestinal bacteria to several organs is reduced by administration of PAF antagonists and that this phenomenon is accompanied by Kupffer cells (KC) hyperplasia. In the present study we compared some functions of hepatic cells and isolated KC from rats with AP to those from healthy animals, treated or not with a PAF antagonist. Materials and Methods AP was induced in Wistar rats by sodium taurocholate (0.5 ml of 2.5% solution) injection into the main pancreatic duct. The animals were killed 24h later, the liver perfused with Krebs solution, non-parenchymal hepatic cells were obtained by Percoll separation and KC by removal of the non-adherent cells. The cells were stimulated or not with LPS (1 mg/mL). Nitrite levels were measured in the supernantants 48h later by Griess reaction and TNF after 6h by bioassay in L929 cells. Microbicidal activity was evaluated by the capacity to kill Candida albicans. The PAF-antagonist WEB2170 (10 mg/kg) was administered iv 30 min before induction of AP. Results: We observed that the non-parenchymal hepatic cells from rats with AP produced higher levels of NO and TNF than those from healthy rats. Stimulation of these cells with LPS increased NO and TNF levels in cells from both, healthy and AP rats. Treatment of the animals with the PAF-antagonist WEB 2170 before induction of pancreatitis, significantly reduced NO but had no effect on TNF production by KC and total hepatic cells. This treatment increased the capacity of KC to kill Candida albicans. Conclusions: These results suggest that PAF released during AP inhibits KC microbicidal activity and this could explain the increased bacterial circulatory dissemination that occurs in AP and the reduction of bacterial translocation observed by using PAF antagonists.