Basic Study
Copyright ©The Author(s) 2018. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Feb 14, 2018; 24(6): 657-670
Published online Feb 14, 2018. doi: 10.3748/wjg.v24.i6.657
Role of PTPN2/22 polymorphisms in pathophysiology of Crohn’s disease
Robert C Sharp, Shazia A Beg, Saleh A Naser
Robert C Sharp, Saleh A Naser, Burnett School of Biomedical Sciences, College of Medicine, University of Central Florida, Orlando, FL 32816, United States
Shazia A Beg, University of Central College of Medicine, Health Center, Orlando, FL 32816, United States
Author contributions: Sharp RC is the primary author who performed all experiments, collected data and participated in writing the manuscript; Beg SA is the clinical coordinator in this study and has supervised recruitment of subjects, collection of clinical samples and transmitting of relevant data to the investigators. She played a vital role in analyzing the data and revising the manuscript; Naser SA is the leading investigator in the lab and has supervised all aspects of the study including writing and editing of the manuscript.
Supported by the Florida Legislative Grant and the Crohn’s Disease Grant Funded by the State of Florida (in part).
Institutional review board statement: The study was approved by the University of Central Florida Institutional Review Board #IRB00001138. Each subject completed and signed a written consent form before samples were collected. Each subject signed a written consent form for publication purposes.
Conflict-of-interest statement: The authors declare that they have no competing interests.
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:
Correspondence to: Saleh A Naser, PhD, Professor, Associate Director, Burnett School of Biomedical Sciences, College of Medicine, University of Central Florida, 4110 Libra Drive, Orlando, FL 32816, United States.
Telephone: +1-407-8230955 Fax: +1-407-8230955
Received: December 20, 2017
Peer-review started: December 21, 2017
First decision: December 27, 2017
Revised: January 3, 2018
Accepted: January 18, 2018
Article in press: January 18, 2018
Published online: February 14, 2018
Core Tip

Core tip: Knowledge of the pathophysiology of Crohn’s disease (CD) is vital in the development of new diagnosis techniques and treatments for the disease. Our study involves the investigation of single nucleotide polymorphisms (SNPs) in protein tyrosine phosphatase non-receptor type 2 and 22 (PTPN2/22) and their effects on susceptibility to mycobacteria species and the elevation of pro-inflammatory cytokines. Our data demonstrates that SNPs in PTPN2/22 lead to less negative regulation in T-cells and increase susceptibility to mycobacteria, thus increasing inflammation and apoptosis in intestinal tissues. Personalized treatment could be accomplished by genetic testing and antibiotic treatment for mycobacteria in CD patients.