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World J Gastroenterol. Mar 14, 2015; 21(10): 2883-2895
Published online Mar 14, 2015. doi: 10.3748/wjg.v21.i10.2883
To be or not to be: The host genetic factor and beyond in Helicobacter pylori mediated gastro-duodenal diseases
Dipanjana Datta De, Susanta Roychoudhury
Dipanjana Datta De, R and D Division (Genetics), School of Human Genetics and Population Health, Kolkata 700012, India
Susanta Roychoudhury, Cancer Biology and Inflammatory Disease Division, Indian Institute of Chemical Biology, Kolkata 700032, India
Author contributions: Datta De D and Roychoudhury S equally contributed to this paper.
Conflict-of-interest: The authors have no conflict of interest related to the manuscript.
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: Susanta Roychoudhury, Chief Scientist, Cancer Biology and Inflammatory Disease Division, Indian Institute of Chemical Biology, 4, Raja S.C Mullick Road, Kolkata 700032, India. susanta@iicb.res.in
Telephone: +91-332-4995823 Fax: +91-332-4735197
Received: July 4, 2014
Peer-review started: July 4, 2014
First decision: August 6, 2014
Revised: August 28, 2014
Accepted: January 8, 2015
Article in press: January 8, 2015
Published online: March 14, 2015
Processing time: 255 Days and 18 Hours
Abstract

Helicobacter pylori (H. pylori) have long been associated with a spectrum of disease outcomes in the gastro-duodenal system. Heterogeneity in bacterial virulence factors or strains is not enough to explain the divergent disease phenotypes manifested by the infection. This review focuses on host genetic factors that are involved during infection and eventually are thought to influence the disease phenotype. We have summarized the different host genes that have been investigated for association studies in H. pylori mediated duodenal ulcer or gastric cancer. We discuss that as the bacteria co-evolved with the host; these host gene also show much variation across different ethnic population. We illustrate the allelic distribution of interleukin-1B, across different population which is one of the most popular candidate gene studied with respect to H. pylori infections. Further, we highlight that several polymorphisms in the pathway gene can by itself or collectively affect the acid secretion pathway axis (gastrin: somatostatin) thereby resulting in a spectrum of disease phenotype

Keywords: Helicobacter pylori; Gastric cancer; Duodenal ulcer; Cytokine; Acid secretion

Core tip:Helicobacter pylori infection results in diverse clinical outcomes. While duodenal ulcer is characterized by hyperacidity, gastric cancer results in hypoacidity. Virulence factors of the bacteria and its own genetic heterogeneity variability does not explain the divergent spectrum of disease manifestation. In this review, we highlight the host genetic factors that are involved and elicited by the bacteria. We discuss the different association studies performed with respect to gastric cancer and duodenal ulcer and further delineate the signaling cue of these inflammatory response pathway gene products to the gastrin: somatostatin axis that is known to regulate acid secretion.