Published online Jun 7, 2016. doi: 10.3748/wjg.v22.i21.4988
Peer-review started: January 18, 2016
First decision: February 18, 2016
Revised: March 21, 2016
Accepted: April 7, 2016
Article in press: April 7, 2016
Published online: June 7, 2016
Core tip: Currently there is no reliable model for chronic multiorgan inflammatory and fibrosis. Tumor necrosis factor (TNF)α initiates inflammation through TNFR1/R2. TNFR1/R2 deficient mice administered orally with dibutyltin dichloride (DBTC) developed significant persistent inflammatory and pain related secondary mechanical hypersensitivity. DBTC-animals showed severe chronic hepatobiliary injuries and prominent biliary ductal dilation. Extensive fibrotic thickening was evidenced around portal ducts, in hepatic and pancreatic structures. DBTC-animals had severe pancreatic damage and pancreatitis, hepatic lesions with expansion of gall bladder, bile stones and severe colitis. This is the first report of chronic inflammatory multiorgan hepatobiliary pancreatitis, fibrosis and calculi formation in TNFR1/R2 deficient mice.