Lipopolysaccharide induced apoptosis of rat pancreatic acinar cells.

BACKGROUND: Bacterial lipopolysaccharide (LPS) has been proposed to participate in the pathogenesis of pancreatic inflammatory disease. AIMS: This study investigated the role of endotoxaemia in the pathogenesis of pancreatic acinar cell injury. METHODS: Sixty eight male Spraque-Dawley rats were used in the study. Escherichia coli LPS (5 mg/kg) was injected into the peritoneal cavity of the rats. The concentration of pancreatic phospholipase A2 (PLA2) in plasma was measured and pancreatic tissue examined by histology, in situ detection of free DNA 3'-ends, and electrophoretic DNA analysis. RESULTS: The concentration of pancreatic PLA2 increased in plasma and the catalytic activity of PLA2 increased in pancreatic tissue after an LPS injection. Apoptosis in pancreatic acinar cells and fragmentation of DNA typical of apoptosis in pancreatic tissue was seen 24 hours after an LPS injection. Pancreatic acinar atrophy was seen 72 hours after the LPS injection. CONCLUSIONS: These data show that LPS causes release of pancreatic PLA2 into blood plasma, activation of PLA2 in pancreatic tissue, and apoptosis of acinar cells.

Phospholipase A2 in sodium taurocholate-induced experimental hemorrhagic pancreatitis in the rat.

We investigated the concentration of immunoreactive pancreatic phospholipase A2 (pan-PLA2) and the catalytic activity of phospholipase A2 (CA-PLA2) in plasma, peritoneal fluid, and pancreas of rats in which acute hemorrhagic pancreatitis was induced by an intraductal injection of sodium taurocholate. The contribution of pancreas to the CA-PLA2 in plasma was studied by removing pancreatic PLA2 by absorbing plasma samples with a polyclonal antibody raised in a rabbit against rat pancreatic PLA2. Sodium taurocholate injected into the pancreatic duct produced hemorrhagic pancreatitis with necrosis and inflammatory cell invasion within 8 hr. Saline injection caused edematous pancreatitis, but sham operation did not alter pancreatic morphology from normal. The concentration of pan-PLA2 increased rapidly in plasma in all animals, but significantly more in sodium taurocholate-injected animals than in saline-injected or sham-operated animals. The level of CA-PLA2 in plasma increased in sodium taurocholate-injected animals only. There was no correlation between pan-PLA2 and CA-PLA2 values in plasma in sodium taurocholate-injected animals. The CA-PLA2 was marginally increased in pancreatic tissue of sodium taurocholate-injected animals compared to that of saline-injected and sham-operated animals at 8 hr. Treatment by the anti-pan-PLA2 antibody effectively removed pan-PLA2 from plasma and peritoneal fluid samples in sodium taurocholate-injected animals. The level of CA-PLA2 in plasma was similar before and after antibody treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Group I and group II phospholipases A2 in serum in uraemia.

Time-resolved fluoroimmunoassays were used for the detection of pancreatic group I and synovial-type group II phospholipases A2 in sera of patients suffering from chronic renal failure before and after haemodialysis. The concentration of group I phospholipase A2 was ten-fold higher in sera of uraemic patients than in healthy controls. There was no significant difference in the concentrations of group I phospholipase A2 in serum before and after haemodialysis. The concentration of group II phospholipase A2 was only marginally increased in sera of uraemic patients, compared with healthy controls. There was no significant difference in the concentrations of group II phospholipase A2 before and after haemodialysis. The results indicate that the metabolism of group I phospholipase A2 differs from that of group II phospholipase A2 in chronic renal failure.