Nuclear Factor-κB in Pancreatitis: Jack-of-All-Trades, But Which One Is More Important?  Ilya Gukovsky, Anna Gukovskaya  Gastroenterology  Volume 144, Issue 1, Pages 26-29 (January 2013) DOI: 10.1053/j.gastro.2012.11.016 Copyright © 2013 AGA Institute Terms and Conditions

Figure 1 Pathways through which acinar cell NF-κB activation regulates inflammation in pancreatitis. A major proinflammatory mechanism is the induction of cytokines and other mediators, as emphasized by Huang et al.21 In contrast, Neuhöfer et al20 emphasize the protective effect of NF-κB against acinar cell necroptosis, limiting pancreatic inflammation. The mechanisms underlying this prosurvival effect of NF-κB are not clear but may involve PAP1,19 Spi2A,20 Bcl-xL,35 and other proteins. One mechanism whereby acinar cell necrosis may promote pancreatic inflammation is through activation of the inflammasome.22,23 The protective effect of NF-κB activation could also be through limiting IL-1β processing and secretion.24 Gastroenterology 2013 144, 26-29DOI: (10.1053/j.gastro.2012.11.016) Copyright © 2013 AGA Institute Terms and Conditions