Published online Nov 6, 2016. doi: 10.4292/wjgpt.v7.i4.540
Peer-review started: May 2, 2016
First decision: July 4, 2016
Revised: July 14, 2016
Accepted: August 15, 2016
Article in press: August 17, 2016
Published online: November 6, 2016
Processing time: 182 Days and 17.7 Hours
Core tip: The use of A20-deficient mice and RNA interference technologies has revealed that mice or enterocytes lacking A20 showed hyper-responsiveness to stimulation. However, studies on whether the overexpression of A20 can extenuate enterocyte inflammation are limited. Our present results demonstrated that the expression of A20 was increased in a dose- and time-dependent manner upon lipopolysaccharide (LPS) stimulation in intestinal epithelial cells. More importantly, the overexpression of A20 suppressed the activation of nuclear factor-κB and the induction of pro-inflammatory molecules, such as Tumor necrosis factor-α and IL-8. Taken together, these findings indicate that A20 plays a critical role in limiting LPS-induced inflammation in the gut luminal and may be a potential therapeutic tool for immune and inflammatory diseases.