Oz HS. Multiorgan chronic inflammatory hepatobiliary pancreatic murine model deficient in tumor necrosis factor receptors 1 and 2. World J Gastroenterol 2016; 22(21): 4988-4998 [PMID: 27275091 DOI: 10.3748/wjg.v22.i21.4988]
Corresponding Author of This Article
Helieh S Oz, DVM, PhD, AGAF, Department of Physiology and Internal Medicine, College of Medicine, University of Kentucky Medical Center, Lexington, KY 40536, United States. hoz2@email.uky.edu
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Basic Study
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Gastroenterol. Jun 7, 2016; 22(21): 4988-4998 Published online Jun 7, 2016. doi: 10.3748/wjg.v22.i21.4988
Multiorgan chronic inflammatory hepatobiliary pancreatic murine model deficient in tumor necrosis factor receptors 1 and 2
Helieh S Oz
Helieh S Oz, Department of Physiology and Internal Medicine, College of Medicine, University of Kentucky Medical Center, Lexington, KY 40536, United States
Author contributions: Oz HS designed and executed the study, prepared the paper and provided funding; author has approved the final paper.
Supported by The NIH grant R03-DE019177.
Institutional animal care and use committee statement: All animal procedures were approved by the University of Kentucky Institutional animal care and use committee.
Conflict-of-interest statement: Author declares to have no commercial or associative interest that represents a conflict of interest in connection with the work submitted.
Data sharing statement: No additional data are available.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Helieh S Oz, DVM, PhD, AGAF, Department of Physiology and Internal Medicine, College of Medicine, University of Kentucky Medical Center, Lexington, KY 40536, United States. hoz2@email.uky.edu
Telephone: +1-859-2770988 Fax: +1-859-3231000
Received: January 15, 2016 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 Processing time: 136 Days and 1.3 Hours
Core Tip
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.
