Ichiro Hirata

Serial change of gastric mucosa after challenging with Helicobacter pylori in the cynomolgus monkey.

The aim of this study was to clarify the change of the gastric mucosa following inoculation with Helicobacter pylori (H. pylori). Two pairs of cynomolgus monkeys received either H. pylori of human origin (group A) or H. pylori of monkey origin (group B) by intragastric inoculation at a dose of 10(9) CFU. After inoculation, endoscopical observation and biopsies were done every 7 days for one month. The bacteria in the biopsy samples were cultured quantitatively. The content of intracellular PAS-AB positive substance was quantitatively analyzed with the image analyzing system. Results were as follows: 1) Before inoculation, the gastric mucosa was endoscopically normal and free from H. pylori. 2) The quantity of H. pylori varied from 0 to 10(3) CFU/0.1 g tissue in group A and from 10 to 10(6) CFU/0.1 g tissue in group B. 3) Severe erosion was seen in group B, while mild mucosal erythema and erosion were observed in group A. 4) There was a correlation between the quantity of H. pylori and histological activity (Rauws gastritis score). 5) The PAS-AB positive substance in H. pylori-positive mucosa was less than that in H. pylori-negative mucosa. In conclusion, gastric mucosal changes of varying degrees were brought about after inoculation of H. pylori depending on the quantity of bacilli in the gastric tissue.

Is Helicobacter pylori a causal agent in gastric carcinoma

The aim of this study is to clarify the relationship between Helicobacter pylori (H. pylori) infection and gastric carcinoma. 94 patients with gastric carcinoma and 111 patients with chronic gastritis were involved in this study. They were classified into 3 age groups: Group A (40 years and under), Group B (41-59), Group C (60 years and over). Serum samples were tested for H. pylori IgG antibodies by ELISA and for pepsinogen (PG) by RIA. The ratio of PG I/PG II was used as a marker for atrophic gastritis. Results were as follows. In the incidence of H. pylori antibodies, there was no significant differences between gastric carcinoma and chronic gastritis in any of the groups. In the quantity of H. pylori antibodies, there was no significant difference between gastric carcinoma and chronic gastritis in any of the groups. The ratio of PG I/PG II was significantly decreased in H. pylori positive cases when compared to H. pylori negative cases in each group with chronic gastritis and group A and B with gastric carcinoma. The ratio of PG I/PG II in gastric carcinoma was significantly lower than that of chronic gastritis. As conclusion, from the point of view of the prevalence of H. pylori, it is suggested that H. pylori is not a direct causal agent in the pathogenesis of gastric carcinoma.

HTLV-Iの母子感染初期にみられた血中IL-2およびsIL-2Rの増加について

In our laboratory, children born to women are known to be infected with Human T-cell Leukemia Virus type-1 (HTLV-I) have been followed using, detect of gene by PCR and antibody by Western Blot Assay (WB) and Immunofluorescence Assay (IFA) test from 1990 through 1996. Four children out of 123 delivery cases have been confirmed to be infected with HTLV-I. We analyzed the correlation between the concentration of cytokines (IL-2, sIL-2R, IFN-gamma) and HTLV-I infection. IL-2 and sIL-2R in sera increased after HTLV-I infection. There was no correlation between the concentration of IFN-gamma and HTLV-I infection. These result suggested that detection of IL-2 and sIL-2R might be the marker of HTLV-I infection.