reported that serum PG I and II level, but not PG I/II ratio, were significantly higher in serum CagA antibody positive compared with negative children.[26] Serum PG was reported to be correlated with gastric inflammatory score.[27] In addition, the cagA status was reported to be associated with various kinds of cytokines including interleukin-8 (IL-8) and may cause severe inflammation

in the stomach.[28] It is also possible that gastritis increases Seliciclib supplier permeability of the gastric epithelial surface, enabling back diffusion of PGs after secretion.[27] These findings suggest that serum CagA antibody titer was associated with gastric inflammation, but not atrophy. Shimoyama et al. reported that inflammation in the antrum and the corpus was more significant in serum CagA antibody positive when they examined the presence of serum CagA antibody by

immunoblot.[29] In the present study, although there were no significant differences of each histological score between serum CagA antibody positive and negative KU-60019 manufacturer group, the mucosal inflammation in the corpus was significantly correlated with serum CagA antibody titer. This finding also supported that different level of antibody production from lymphocytes induced by H. pylori infection can contribute to the various serum CagA antibody level. Interestingly, positive correlation between the inflammatory score and serum CagA antibody titer was found only in the corpus but not in the antrum. Corpus dominant gastritis rather than antrum dominant gastritis was a risk factor to develop gastric ulcer and gastric cancer.[3, 30] In addition, even when only serum CagA antibody positive group was selected, serum CagA antibody titer was significantly correlated with inflammation and activity in the corpus. Therefore, antibody titer rather than the presence of antibody can be a useful marker for advanced inflammation in the stomach in Japan. This suggests that serum CagA antibody titer might be an available marker to predict click here a gastric cancer in Japan. It has also been reported that measurement of serum levels of C-reactive protein (CRP) using a high-sensitivity assay (hs-CRP) can reveal

subclinical inflammatory states that may reflect vascular inflammation.[31] Recent report showed that the mean serum level of hs-CRP was significantly higher in H. pylori-positive group than H. pylori-negative group, although the level of hs-CRP was not different between CagA antibody positive and negative group in Iran.[32] It is better to examine the association between serum CagA antibody and hs-CRP in Japan in the further study. In our study, in spite of cagA positive by PCR, the prevalence of serum CagA antibody was 75.0%, which was consistent with previous studies from Japan.[17, 33] The cagA gene is located at one end of the cag pathogenicity island (PAI), an approximately 40-kbp region that is thought to have been incorporated into the H. pylori genome by horizontal transfer from an unknown source.