Isolates that were indeterminate in one or more regions (n = 9) were excluded from this compilation. Figure 4 Summary of the vacA gene mosaic combinations based on amplicon sequencing

in 145 biopsies. Genotypes in the remaining 14 biopsies could not be established. N = number of strains; s1/s2, signal-sequence type; i1/i2 = intermediate region type; d1/d2 = deletion type; m1/m2 = mid-region type. In group 3, there were two isolates Gamma-secretase inhibitor (6%) derived from peptic ulcer patients, while in group 1 and 2 there were 20 isolates (24%) and eight isolates (27%), respectively, originating from ulcer patients. The lower frequency of peptic ulcer observed in vacA s1d1m1 genotype compared to other genotypes was not statistically significant. Eight biopsies from group 1 (10%) and two biopsies from group 2 (7%) were derived from patients with

atrophic gastritis, while in group three there was no subject with atrophic gastritis (not statistically significant). Intraindividual variations of cagA EPIYA and vacA genotypes in corpus, antrum and duodenal bulb In 51 of 71 individuals, Selleckchem p38 MAPK inhibitor biopsy specimens from all three locations of the stomach (corpus, antrum and duodenal bulb) were available for analysis. In 26 of these 51 subjects, the cagA and vacA genotypes were identical in all locations. Considering the remaining 25 subjects, 22 subjects differed with respect to the cagA EPIYA genotype, two with regard to the vacA (i) genotype, two considering

the vacA (d) genotype and one with respect to the vacA (m) genotype, when comparing the locations for each subject (Additional file 1). Discussion The results of several studies have indicated that Flavopiridol (Alvocidib) there is an association between the cagA gene and gastric cancer [14, 27, 28, 48]. There are also reports showing an association between the vacA gene and gastroduodenal sequelae (e.g. peptic ulcer, atrophic gastritis) of H. pylori infection [36, 38–40]. Here we show that of the individuals with biopsies from all locationsns (corpus, antrum and duodenal bulb), 49% had different cagA EPIYA genotype between the three locations. There is a possibility that these individuals may have been infected with different strains on different occasions. However, it is perhaps more likely those H. pylori strains acquired genetic alterations in cagA after infection. Three recombination mechanisms have been detected in the cagA gene; homologous recombination between CM sequences, recombination between EPIYA sequences or between short similar sequences [49]. These recombination mechanisms, as well as mutations in the gene, may serve as a driving force for generating strain diversity in H. pylori, also called microevolution [50]. It is possible that infection with multiple H.