Endotoxemia in the infant rats modulates HSP60 protein level in the pancreatic acinar cells.

Lipopolysaccharide (endotoxin, LPS) is responsible for septic shock and multiorgan failure, but pretreatment of the rats with low doses of LPS reduced pancreatic damage produced by caerulein-induced pancreatitis (CIP). In spite of this observations the effects of LPS and caerulein on pro-apoptotic HSP60 and Bax protein expression in the pancreatic acinar cells has not been examined yet. The aim of this study was to assess the effects of endotoxemia induced in the early period of life on the pro-apoptotic nuclear HSP60 and mitochondrial Bax protein expressions detected in the pancreas of adult animals. Newborn rats (25 g) were injected with endotoxin (Escherichia coli) for 5 consecutive days, at the total doses of 25, 50 or 75 mg/kg. Control animals received injections of physiological saline. Two months later the pancreatic acinar cells were isolated from all above groups of rats and subjected to caerulein over stimulation (10(-8)M). Total nuclear HSP60 and mitochondrial Bax protein expression were isolated for Western blot and co-immunoprecipitation studies. High levels of pro-apoptotic nuclear HSP60 and mitochondrial Bax protein has been observed in the pancreatic acinar cells under basal conditions. Pretreatment of newborn rats with LPS failed to affect significantly the HSP60 and Bax protein levels in the pancreatic acini isolated from the same animals 2 months later, as compared to the control group. Caerulein stimulation significantly reduced the level of these proteins. Pretreatment of suckling rats with LPS (at the total doses of 25, 50 or 75 mg/kg) reversed above caerulein-induced suppression of pro-apoptotic nuclear HSP60 and mitochondrial Bax protein levels in the pancreatic acini obtained from adult rats. We conclude that pretreatment of suckling rats with LPS reversed the suppression of pro-apoptotic HSP60 and Bax protein levels produced by caerulein overstimulation in the pancreatic acini. This mechanism could take a part in the LPS-induced protection of the pancreatic tissue against acute damage.