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Gastroenterology Research and Practice
Volume 2015 (2015), Article ID 141070, 17 pages
Review Article

Role of TLR4  rs4986790A>G and rs4986791C>T Polymorphisms in the Risk of Inflammatory Bowel Disease

1Department of Gastroenterology, First Affiliated Hospital of China Medical University, Shenyang 110001, China
2Department of Pathophysiology, College of Basic Medical Sciences, China Medical University, Shenyang 110001, China

Received 16 January 2015; Revised 8 April 2015; Accepted 15 April 2015

Academic Editor: Paolo Gionchetti

Copyright © 2015 Ran Ao et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Objective. The present meta-analysis investigated the contribution of TLR4 rs4986790A>G and rs4986791C>T genetic polymorphisms in increasing the risk of inflammatory bowel disease (IBD). Methods. Databases were searched using a combination of keywords related to TLR4 and IBD. Relevant studies were selected based on strict inclusion and exclusion criteria. Meta-analysis of the data extracted from the selected studies was performed using CMA 2.0 statistical analysis software. Results. Out of the 70 studies retrieved by database search, only 13 studies were eligible for inclusion in this meta-analysis and these 13 studies contained a total number of 4409 IBD patients and 5693 healthy controls. The meta-analysis results demonstrated that TLR4 rs4986790A>G polymorphism is associated with an increased risk of IBD (allele model: OR = 1.268, 95% CI = 1.124~1.431, and ; dominant model: OR = 1.240, 95% CI = 1.090~1.409, and ). Similarly, TLR4 rs4986791C>T polymorphism also conferred an increased risk of IBD (allele model: OR = 1.259, 95% CI = 1.092~1.453, and ; dominant model: OR = 1.246, 95% CI = 1.072~1.447, and ). Conclusion. Our meta-analysis results demonstrate that TLR4 rs4986790A>G and rs4986791C>T genetic polymorphisms are associated with the etiopathogenesis of IBD.