Published online Mar 14, 2015. doi: 10.3748/wjg.v21.i10.2883
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
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
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.