November 12, 2014
Notes: Li, Zhi-yu
Research Support, Non-U.S. Gov’t
J Zhejiang Univ Sci B. 2013 Jun;14(6):549-54. doi: 10.1631/jzus.B1200247.
Author Address: Department of Surgery, the Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310009, China.
Reference Type: Journal Article
Record Number: 5127Author: Liang, H. Y., Song, Z. M. and Cui, Z. J.
Title: Lasting inhibition of receptor-mediated calcium oscillations in pancreatic acini by neutrophil respiratory burst–a novel mechanism for secretory blockade in acute pancreatitis?
Journal: Biochem Biophys Res Commun
Date: Aug 2
Short Title: Lasting inhibition of receptor-mediated calcium oscillations in pancreatic acini by neutrophil respiratory burst–a novel mechanism for secretory blockade in acute pancreatitis?
Alternate Journal: Biochemical and biophysical research communications
ISSN: 1090-2104 (Electronic)
Accession Number: 23820383
Keywords: Acetylcholine/*antagonists & inhibitors/physiology
Cell Line, Tumor
Receptors, Cholecystokinin/*antagonists & inhibitors/physiology
alpha7 Nicotinic Acetylcholine Receptor
Abstract: Although overwhelming evidence indicates that neutrophil infiltration is an early event in acute pancreatitis, the effect of neutrophil respiratory burst on pancreatic acini has not been investigated. In the present work, effect of fMLP-induced neutrophil respiratory burst on pancreatic acini was examined. It was found that neutrophil respiratory burst blocked calcium oscillations induced by cholecystokinin or by acetylcholine. Such lasting inhibition was dependent on the density of bursting neutrophils and could be overcome by increased agonist concentration. Inhibition of cholecystokinin stimulation was also observed in AR4-2J cells. In sharp contrast, neutrophil respiratory burst had no effect on calcium oscillations induced by phenylephrine (PE), vasopressin, or by ATP in rat hepatocytes. These data together suggest that inhibition of receptor-mediated calcium oscillations in pancreatic acini by neutrophil respiratory burst would lead to secretory blockade, which is a hallmark of acute pancreatitis. The present work has important implications for clinical treatment and management of acute pancreatitis.