The infection remains latent in the majority of infected patients, only a minority of individuals with infection ever develop it 2. levels (P = 0.003 and 0.004, respectively). Serum CagA 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 CagA antibody titer. CagA expression level of the strains was irrespective of the status of PG and serum CagA antibody. Conclusions Subjects with higher serum CagA 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 Japan. Host recognition rather than bacterial colonization might be associated with the difference of serum CagA antibody titer. is a spiral Gram-negative bacterium that infects more than half of the worlds population 1. infection is now accepted to be linked NVP-BSK805 to severe gastritis-associated diseases, including peptic ulcer and gastric cancer 1. The infection remains latent in the majority of infected patients, only a minority of individuals with infection ever develop it 2. Uemura reported that gastric cancer developed in approximately 3% of strains are related with the varying outcomes of infection. The best studied virulence factor of is the CagA protein. CagA producing strains are reported to be associated with severe clinical outcomes, especially in Western countries 4C7. CagA is a highly immunogenic protein with a molecular weight between 120 and 140 kDa 8, 9. In 2003, Huang performed meta-analysis of the association between CagA seropositivity and gastric cancer 10. They concluded that the infection of CagA positive strains increase the risk of NVP-BSK805 gastric cancer. However, because they included studies from both Western and Asian countries, it was not clear whether an association between CagA seropositivity and gastric cancer really exists in East Asian countries. In East Asian countries, it is difficult to prove the importance of the gene in clinical outcomes because almost all strains possess the gene. For example, we previously examined 491 Japanese strains from a region in the middle of Japan (Kyoto) and found that 96.3% of the strains were gene-positive, NVP-BSK805 irrespective of clinical outcomes 11; similar results have been published for different regions in Japan 12C14 and other countries in East Asia 15, 16. Interestingly, subjects infected with do not always induce serum CagA antibody even in East Asian countries. For example, although most Japanese possess may be a more useful marker to detect the high risk population for severe outcomes in East Asian countries. Intriguingly, we reported that CagA seropositivity was significantly associated with gastric cancer even in East Asian countries in meta-analysis 19. This suggests that anti-CagA antibody can be used as a biomarker for gastric cancer even in East Asian countries. It remains unclear why not all subjects have serum CagA antibody in Japan. As described above, subjects with serum CagA antibody can be considered as a high risk group for gastric cancer. Several factors such as bacterial factors and/or host recognition of CagA, and environmental factors may affect the difference of serum CagA antibody titer. In addition, it is not clear why serum CagA positive is associated with gastric cancer. In this study, we aimed to examine the relationship between anti CagA antibody titer and the levels of pepsinogen (PG), and histological score. Methods Patients Patients were considered to be culture and histopathologic examination. Written informed consent was obtained from all participants, and the protocol was approved by the Ethics Committee of Oita University. ELISA for serum CagA antibody titer and pepsinogen Serum anti CagA IgG antibody was measured by using a commercially available enzyme-linked immunosorbent assay (ELISA) kit Rabbit Polyclonal to CLCNKA (Genesis Diagnostics Ltd, Cambridgeshire, UK). Equal and more than 6.25 U/mL was defined as positive based on the manufacturers instructions. The level of the serum PG I and PG II were measured by Pepsinogen ELISA kit (Eiken, Co. Ltd., Tokyo, Japan) according to the manufacturers instructions. Histological analysis All biopsy materials were fixed in 10% buffered formalin for 24 h, then embedded in paraffin. Serial sections were stained with hematoxylin and eosin and with MayCGiemsa stain. State of the gastric mucosa was evaluated according to the updated Sydney system 20. The degree of inflammation, neutrophil activity,.