Published online Apr 14, 2015. doi: 10.3748/wjg.v21.i14.4293
Peer-review started: November 12, 2014
First decision: December 11, 2014
Revised: January 11, 2015
Accepted: February 5, 2015
Article in press: February 5, 2015
Published online: April 14, 2015
Processing time: 155 Days and 12.5 Hours
AIM: To assess the impact of Arpin protein and tight junction (TJ) proteins in the intestinal mucosa on bacterial translocation in patients with severe acute pancreatitis (SAP).
METHODS: Fifty SAP patients were identified as study objects and then classified into two groups according to the presence of bacterial translocation (BT) in the blood [i.e., BT(+) and BT(-)]. Twenty healthy individuals were included in the control group. BT was analyzed by polymerase chain reaction, colonic mucosal tissue was obtained by endoscopy and the expression of TJ proteins and Arpin protein was determined using immunofluorescence and western blotting.
RESULTS: Bacterial DNA was detected in the peripheral blood of 62.0% of patients (31/50) with SAP. The expression of TJ proteins in SAP patients was lower than that in healthy controls. In contrast, Arpin protein expression in SAP patients was higher than in healthy controls (0.38 ± 0.19 vs 0.28 ± 0.16, P < 0.05). Among SAP patients, those positive for BT showed a higher level of claudin-2 expression (0.64 ± 0.27 vs 0.32 ± 0.21, P < 0.05) and a lower level of occludin (OC) (0.61 ± 0.28 vs 0.73 ± 0.32, P < 0.05) and zonula occludens-1 (0.42 ± 0.26 vs 0.58 ± 0.17, P = 0.038) expression in comparison with BT (-) patients. Moreover, the level of Arpin expression in BT (+) patients was higher than in BT (-) patients (0.61 ± 0.28 vs 0.31 ± 0.24, P < 0.05).
CONCLUSION: Arpin protein affects the expression of tight junction proteins and may have an impact on BT. These results contribute to a better understanding of the factors involved in bacterial translocation during acute pancreatitis.
Core tip: Tight junctions (TJs) are the structural basis for the intestinal epithelial barrier. Increased intestinal permeability caused by variations in TJ proteins may result in bacterial translocation (BT) and there is evidence that BT may contribute to infection and sepsis. However, the detailed mechanisms for BT remain unknown. Recent work has identified an Arp2/3 interacting protein called Arpin, which was shown to restrict the rate of actin polymerization and control cell migration. Our research shows that Arpin protein affects the expression of TJ proteins and may have an impact on BT.