| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
B
1 Department of Pharmacology, National University of Singapore, United States
2 Department of Pharmacology, National University of Singapore, Singapore, Singapore
* To whom correspondence should be addressed. E-mail: mbhatia{at}nus.edu.sg.
Acinar cell injury early in acute pancreatitis leads to a local inflammatory reaction and to the subsequent systemic inflammatory response, which may result in multiple organ dysfunction and death. Inflammatory mediators including chemokines and substance P (SP) are known to play a crucial role in the pathogenesis of acute pancreatitis. It has been shown that pancreatic acinar cells produce the chemokine MCP-1 in response to caerulein hyperstimulation, demonstrating that acinar-derived MCP-1 is an early mediator of inflammation in acute pancreatitis. Similarly SP levels in the pancreas and pancreatic acinar cell expression of NK-1R, the primary receptor for SP, are both increased during secretagogue-induced experimental pancreatitis.This study aims to examine the functional consequences of exposing mouse pancreatic acinar cells to SP and determine if it leads to proinflammatory signalling such as production of chemokines. Exposure of mouse pancreatic acini to SP significantly increased synthesis of CC chemokine MCP-1 and MIP-1
as well as CXC chemokine MIP-2.Furthermore SP also increased NF-
B activation. The stimulatory effect of SP was specific to chemokine synthesis through the NF-B pathway, since the increased in chemokine production was completely attenuated when pancreatic acini were pre-treated with the selective NF-B inhibitor, Nemo binding domain peptide. This study shows that SP-induced chemokine synthesis in mouse pancreatic acinar cells is NF-B dependent.
This article has been cited by other articles:
|
|
 |
|
  Y.-H. Koh, R. Tamizhselvi, and M. Bhatia Extracellular Signal-Regulated Kinase 1/2 and c-Jun NH2-Terminal Kinase, through Nuclear Factor-{kappa}B and Activator Protein-1, Contribute to Caerulein-Induced Expression of Substance P and Neurokinin-1 Receptors in Pancreatic Acinar Cells J. Pharmacol. Exp. Ther., March 1, 2010; 332(3): 940 - 948. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. D. Ramnath, J. Sun, and M. Bhatia Involvement of Src Family Kinases in Substance P-Induced Chemokine Production in Mouse Pancreatic Acinar Cells and Its Significance in Acute Pancreatitis J. Pharmacol. Exp. Ther., May 1, 2009; 329(2): 418 - 428. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Sun, R. D. Ramnath, R. Tamizhselvi, and M. Bhatia Neurokinin A engages neurokinin-1 receptor to induce NF-{kappa}B-dependent gene expression in murine macrophages: implications of ERK1/2 and PI 3-kinase/Akt pathways Am J Physiol Cell Physiol, September 1, 2008; 295(3): C679 - C691. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. L. Rittner, A. Brack, and C. Stein Pain and the immune system Br. J. Anaesth., July 1, 2008; 101(1): 40 - 44. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. D. Ramnath, J. Sun, S. Adhikari, L. Zhi, and M. Bhatia Role of PKC-{delta} on substance P-induced chemokine synthesis in pancreatic acinar cells Am J Physiol Cell Physiol, March 1, 2008; 294(3): C683 - C692. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Sun, R. D. Ramnath, and M. Bhatia Neuropeptide substance P upregulates chemokine and chemokine receptor expression in primary mouse neutrophils Am J Physiol Cell Physiol, August 1, 2007; 293(2): C696 - C704. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. D. Baumler, D. W. Nelson, D. M. Ney, and G. E. Groblewski Loss of exocrine pancreatic stimulation during parenteral feeding suppresses digestive enzyme expression and induces Hsp70 expression Am J Physiol Gastrointest Liver Physiol, March 1, 2007; 292(3): G857 - G866. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
