Acinar Tight Junctions are Altered in an Early Phase of Acute Edematous Pancreatitis in a Rat Pancreatic Duct Ligation Model

Background: Although trypsin autoactivation in acinar cells is considered to be an initial event in acute human pancreatitis, mild pancreatitis with/without trypsin autoactivation is common in human acute pancreatitis, and interstitial edema is one of its characteristic features.Methods: To elucidate the mechanism underlying such interstitial edema in acute edematous pancreatitis, we examined the condition of intercellular junction complexes between acinar cells in the initial phase of pancreatitis in a rat pancreatic duct ligation model.For this experiment, serum and pancreatic tissues were obtained at 30, 60, 120, and 180 mins after duct ligation and compared biochemically, morphologically, and immunofluorescently with samples from control or sham-operated rats.Results: In the present experiments, both the tissue water content and the serum amylase values were elevated only in the group 180 min after duct ligation.Tissue trypsin values revealed no significant changes, and histology did not reveal tissue necrosis.In an immunofluorescence study, acinar luminal staining for the tight junction-protein ZO-1 was significantly less distinct in both the groups 120 min and 180 min after duct ligation, although the adherens junction proteins pan-cadherin and β-catenin showed no significant changes throughout the course of the experiment.Ultrastructurally, tight junctions in both groups (120 and 180 mins) appeared leaky (not closed) more frequently than in other groups.Conclusions: Acinar tight junctions were altered in an early phase of pancreatitis in the present acute edematous pancreatitis model, and such alterations may contribute to the interstitial edema formation that is characteristic of mild pancreatitis.