pylori and may play a role in the geographic differences in gastric cancer rates.52,65 BabA is an OMP that functions as an adhesin by binding to Lewis-related antigens, facilitating colonization and induction of mucosal Selleck CH5424802 inflammation. It has been associated with the development of gastroduodenal

diseases, including gastric cancer. However, unlike the oipA gene, there are no obvious differences in genomic structures of the babA gene between Eastern and Western strains.52 The OMP SabA mediates the binding of H. pylori to sialylated structures on neutrophils and erythrocytes. SabA-positive status has been associated with gastric cancer, intestinal metaplasia, and corpus atrophy, and negatively associated with duodenal ulcer.64 AlpAB is another OMP involved in adhesion of H. pylori to gastric mucosa.66 Lu et al. showed that AlpAB was involved in cellular adhesion and that deletion of alpAB reduced IL-6 induction in gastric epithelial cells. Deletion of alpAB reduced IL-8 induction with East Asian strains but not with Western strains. All AlpAB-positive strains see more activated the extracellular signal-regulated kinase, c-Fos, and cAMP-responsive element-binding protein. However, activation of the Jun—N-terminal kinase, c-Jun, and NF-kappaB was exclusive to AlpAB from East Asian strains. These results suggest that the geographic variation in gastric cancer rates could potentially be related to differential

effects of East Asian and Western types of AlpAB.67 The Indian enigma is actually a subset of the Asian enigma, which refers to the observations that there are regions where H. pylori infection is high yet the gastric cancer incidence is relatively low. The data that led to this term were mainly epidemiological. The regions where these observations are made are India, Bangladesh, Pakistan and Thailand. To explain these ‘enigmas’, host genetics, bacterial factors and environmental

factors such as diet have been involved. Recently, it has been suggested that in reality the concept of an ‘Asian enigma’ is flawed, in that these differences in H. pylori strains geographically do not account for the differences in disease manifestation. It has been suggested that disease manifestation reflects the predominant learn more pattern of gastritis within a geographic region, and that the interaction of host genetic factors and environmental factors such as diet are the main factors, rather than the strain of H. pylori.49 However, it would be fairer to acknowledge that there are still gaps in our understanding of the process of gastric carcinogenesis. Furthermore, there is also a lack of data documenting the precise gastric histology in these populations with low gastric cancer but high H. pylori seroprevalence rates. Accepting that the topographical pattern and severity of gastritis is the main reason for the differences in disease type, the question still exists as to why these differences exist.