Presence of iceA1 but not cagA, cagC, cagE, cagF, cagN, cagT, or orf13 genes of Helicobacter pylori is associated with more severe gastric inflammation in Taiwanese

Background and Purpose. The presence Of the cag pathogenicity, island (PAI) may enhance the virulence of Helicobacter pylori. This study determined the prevalence of genotypes of the PAI, IS605, and iceA1 in H. pylori strains in Taiwanese and whether these genotypes were related to the type of clinical disease or gastric pathology. Methods: One hundred clinical isolates were Collected from 33 duodenal ulcer, I I I nonulcer related dyspepsia, 14 gastric ulcer, and 12 gastric malignancy, patients, Polymerase chain reaction (PCR) assays were performed for cagA, cagC, cagE, cagF, arid cagN in the cagI region, cagT arid orf13 ill the cagII region, and IS605 and I iceA1 in all H. pylori isolates. Gastric histology of the infected host was reviewed using the updated Sydney system. Results: All strains were positive for all the selected genes in the PAJ. PCR amplification found IS605 in 17%. while colony hybridization revealed it in 36% of strains. The prevalence of the cagA gene detected by PCR using cagA1, cagA2, and cagA3 printers was 26. 100, arid 100%. respectively. The iceA1 gene existed in 72% of the H. pylori isolates. The mean ulcer size arid the severity of acute gastric inflammation in patients infected with iceA1-positive strains were significantly greater than in those infected with iceA1-negative strains (p < 0.05). Conclusions: All clinical H. pylori isolates front different gastric diseases in our Taiwanese patients were positive for the PAI, but only 36%, of these isolates carried all IS605 insertion. The selected genes in the PAJ were not correlated with disease outcome. The determination of cagA prevalence is based oil the selection Of suitable primers. In contrast, bacterial factors such as the presence of ice,41 could be related to severity of gastric inflammation and increase in ulcer size in II. pylori-infected patients.