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Serum H elicobacter pylori C ag A antibody titer as a useful marker for advanced inflammation in the stomach in J apan
Author(s) -
Shiota Seiji,
Murakami Kazunari,
Okimoto Tadayoshi,
Kodama Masaaki,
Yamaoka Yoshio
Publication year - 2014
Publication title -
journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.214
H-Index - 130
eISSN - 1440-1746
pISSN - 0815-9319
DOI - 10.1111/jgh.12359
Subject(s) - caga , antibody , helicobacter pylori , titer , medicine , antibody titer , immunology , gastritis , population , biology , virulence , gene , biochemistry , environmental health
Background and Aim Subjects infected with H elicobacter pylori containing cagA do not always induce serum C ag A antibody. Our previous meta‐analysis showed that serum C ag A seropositivity was associated with gastric cancer even in E ast A sian countries. However, it remains unclear why serum C ag A ‐positive status is associated with gastric cancer. In this study, we aimed to examine the relationship between anti‐ C ag A antibody titer and the levels of pepsinogen ( PG ), and histological score. Methods Eighty‐eight H . pylori ‐positive Japanese patients with gastritis were included. Serum C ag A antibody titer, PG I , and PG II were evaluated by ELISA . Histological scores were evaluated according to U pdate S ydney System. C ag A expression was examined by immunoblot. Results Seroprevalence of C ag A antibody was found in 75.0%. Interestingly, serum C ag A antibody titer was significantly correlated with PG I and PG II levels ( P = 0.003 and 0.004, respectively). Serum C ag A antibody titer was also significantly correlated with mucosal inflammation in the corpus ( P = 0.04). On the other hand, bacterial density was not related with C ag A antibody titer. C ag A expression level of the strains was irrespective of the status of PG and serum C ag A antibody. Conclusions Subjects with higher serum C ag A antibody titer can be considered as high‐risk population for the development of gastric cancer from the point of strong gastric inflammatory response even in J apan. Host recognition rather than bacterial colonization might be associated with the difference of serum C ag A antibody titer.