November 12, 2014
Notes: Wang, Guiliang
Randomized Controlled Trial
Research Support, Non-U.S. Gov’t
J Surg Res. 2013 Aug;183(2):592-7. doi: 10.1016/j.jss.2012.12.010. Epub 2013 Jan 3.
Author Address: Department of Digestive Internal Medicine, Pingxiang Hospital, Southern Medical University, Pingxiang, Jiangxi, People’s Republic of China.
Reference Type: Journal Article
Record Number: 5154Author: Wang, J., Xu, P., Hou, Y. Q., Xu, K., Li, Q. H. and Huang, L.
Title: Pancreatitis-associated ascitic fluid induces proinflammatory cytokine expression in THP-1 cells by inhibiting anti-inflammatory signaling
Short Title: Pancreatitis-associated ascitic fluid induces proinflammatory cytokine expression in THP-1 cells by inhibiting anti-inflammatory signaling
Alternate Journal: Pancreas
ISSN: 1536-4828 (Electronic)
Accession Number: 23774701
Keywords: Acute Disease
Cell Line, Tumor
Cell Survival/drug effects
Dose-Response Relationship, Drug
Gene Expression/drug effects
Leukemia, Monocytic, Acute/genetics/metabolism/pathology
Reverse Transcriptase Polymerase Chain Reaction
Signal Transduction/*drug effects
Transcription Factor RelA/antagonists & inhibitors/metabolism
Tumor Necrosis Factor-alpha/genetics
p38 Mitogen-Activated Protein Kinases/antagonists & inhibitors/metabolism
Abstract: OBJECTIVES: We investigated whether pancreatitis-associated ascitic fluid (PAAF) could induce the expression of tumor necrosis factor alpha (TNF-alpha) and interleukin 6 (IL-6) in THP-1 cells and the mechanism(s) involved. METHODS: THP-1 cells were divided into control and PAAF groups. The PAAF group was incubated with different final concentrations of PAAF, whereas the control group was incubated with culture medium. Effects and mechanisms were determined by measuring the levels of TNF-alpha and IL-6 mRNA expression; phospho-p38-MAPK, nuclear factor kappaB, peroxisome proliferator-activated receptor gamma activation; and the effect on the inhibitory activity of SB203580 and BAY-117082. RESULTS: In response to PAAF, overexpression of TNF-alpha and IL-6 mRNA was found in THP-1 cells compared with those of the corresponding control (P < 0.05), and in a dose-dependent manner. The levels of phospho-p38 and nuclear factor kappaB p65 were also increased in different PAAF groups, whereas low expression of peroxisome proliferator-activated receptor gamma was found compared with the control group (P < 0.05). Furthermore, we presented that the inflammatory response could be partly alleviated by inhibitors SB203580 or BAY-117082, whereas it was markedly inhibited by the simultaneous treatment of 2 inhibitors. CONCLUSIONS: Pancreatitis-associated ascitic fluid up-regulated proinflammatory cytokines by interfering with proinflammatory and anti-inflammatory signaling pathways, thus exacerbating activation in acute pancreatitis.