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the H. pylori isolates have universal presence of genes in cag-PAI and expression of CagA [13–16]. On the basis of the semi-quantitative analysis of the translocated p-CagA bands in the western blots, the strains in this study have diverse intensity of p-CagA. To further evaluate the clinical impact of the diverse p-CagA intensity on the clinical outcome, we selected a clinical strain with marked p-CagA to serve as reference index to subgroup the 146 collected strains according to their p-CagA intensity into strong, weak, or sparse. Based on this categorization, this study showed that H. pylori isolates with stronger p-CagA SB431542 research buy were correlated to more severe gastric inflammation and an increased risk of gastric IM and cancer. The possible factors to affect CagA phosphrylation include the cagA genotype, type IV secretion system, the CagA EPIYA-repeat motif of the strain, and the adhesion phenotype of the epithelial cell [22–27]. Animal

studies have shown that mutant strains of CagA, CagE, or CagY could reduce the gastric inflammation p38 MAPK inhibitor after infection [10, 28]. Moreover, the CagA EPIYA polymorphism has also a causal role in clinical outcome [18, 29]. These data support that these factors are all important in the H. pylori related gastric inflammation via CagA phosphorylation. However, there is no previous human study to evaluate the impact of the p-CagA intensity on gastric histological changes. Thus, this study is first time to disclose that strains isolated from gastric cancer and IM patients had a stronger p-CagA function as compared with strain from gastritis without IM patients (Figure 2). However, those were not significantly stronger than the strains from gastric or duodenal ulcer. This result can be explained that the IM and non-IM were both included into the gastric and duodenal ulcer subgroups to dilute the

significance. This explanation may be also supported by a study Go6983 showing that the intensities of p-CagA were not significantly different among different clinical diseases [22]. Moreover, as shown in Figure 3, the isolates from patients with cancer risk (i.e, patients of with IM or cancer) had significantly stronger p-CagA intensity than those from patients without cancer risk (p < 0.001). This data further support that strong p-CagA increase the risk of developing gastric carcinogenesis from H. pylori infection. Furthermore, the patients with IM or cancer had severer acute and chronic inflammation in gastric histology. Also shown in Figure 4, the patients infected with stronger p-CagA H. pylori strains could correlate with severer acute or chronic gastritis (p < 0.05). This indicated that the p-CagA intensity is closely related to provoke gastric inflammation in both patients with and without gastric cancers. It is well known that the H.