OBJECTIVE: The aim of the present study was to determine the underlying cellular mechanisms in the pancreas after acute pancreatitis and to study the pathogenesis of pancreatitis-associated lung injury. We applied a differential display analysis to normal pancreas and to the pancreas with acute pancreatitis in rats, and we examined the expression of the identified gene in the lung as well as the pancreas after acute pancreatitis. DESIGN: Controlled animal study. SETTING: Research laboratory of an academic institution. SUBJECTS: Ninety male Wistar rats. INVESTIGATIONS: Pancreatitis was induced by retrograde intraductal infusion of 4% sodium taurocholate (100 microL/100 g of body weight). Data were compared with data from controls (sham). MEASUREMENTS AND MAIN RESULTS: We cloned some expressed sequence tags and identified one complementary DNA fragment. The deduced protein was a polypeptide of 218 amino acids, which was almost identical to human 19-kD interacting protein-3-like (NIP3L) protein. The expression of rat NIP3L identified in this study increased slightly in the pancreas after induction of acute pancreatitis but showed a marked increase in the lung by both Northern and Western blot analysis. NIP3L immunoreactivity was noted in alveolar and epithelial cells of the control (sham) lung, and the immunoreactivity in these cells was elevated after induction of acute pancreatitis. Moreover, acute pancreatitis increased terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling-positive alveolar and bronchiolar cells in the lung. CONCLUSION: NIP3L may be involved in lung injury, which is one of the major causes of death in cases of severe acute pancreatitis.
OBJECTIVE: The aim of the present study was to determine the underlying cellular mechanisms in the pancreas after acute pancreatitis and to study the pathogenesis of pancreatitis-associated lung injury. We applied a differential display analysis to normal pancreas and to the pancreas with acute pancreatitis in rats, and we examined the expression of the identified gene in the lung as well as the pancreas after acute pancreatitis. DESIGN: Controlled animal study. SETTING: Research laboratory of an academic institution. SUBJECTS: Ninety male Wistar rats. INVESTIGATIONS: Pancreatitis was induced by retrograde intraductal infusion of 4% sodium taurocholate (100 microL/100 g of body weight). Data were compared with data from controls (sham). MEASUREMENTS AND MAIN RESULTS: We cloned some expressed sequence tags and identified one complementary DNA fragment. The deduced protein was a polypeptide of 218 amino acids, which was almost identical to human 19-kD interacting protein-3-like (NIP3L) protein. The expression of ratNIP3L identified in this study increased slightly in the pancreas after induction of acute pancreatitis but showed a marked increase in the lung by both Northern and Western blot analysis. NIP3L immunoreactivity was noted in alveolar and epithelial cells of the control (sham) lung, and the immunoreactivity in these cells was elevated after induction of acute pancreatitis. Moreover, acute pancreatitis increased terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling-positive alveolar and bronchiolar cells in the lung. CONCLUSION:NIP3L may be involved in lung injury, which is one of the major causes of death in cases of severe acute pancreatitis.