Invasiveness of Helicobacter pylori into human gastric mucosa.

BACKGROUND: Helicobacter pylori has generally been observed only in the gastric mucous layer or in the spaces between gastric mucus-secreting cells and not in the gastric epithelial cells or in the lamina propria. The purpose of this study is to determine whether H. pylori invades the gastric mucosa, using an immunoelectron microscopical examination of human gastric mucosa infected with H. pylori. MATERIALS AND METHODS: Five hundred gastric antral biopsy specimens were fixed in a periodate-lysin-paraformaldehyde solution, embedded in Lowicryl, sectioned, and examined with a light microscope. One hundred specimens moderately or severely infected with H. pylori were selected and were incubated with polyclonal rabbit anti-H. pylori antibody. The specimens were washed, incubated with 20 nm of colloidal gold-conjugated goat anti-rabbit IgG, stained with uranyl acetate and lead citrate, and observed with a transmission electron microscope. RESULTS: In one case, a bacterium was observed within the cytoplasm of a gastric mucus-secreting cell; in another case, a few bacteria were observed within the cytoplasm of a stromal cell in the lamina propria. The bacteria could be differentiated from degenerated intracellular organelles by gold particles attached to the bacteria. CONCLUSION: H. pylori rarely invade the lamina propria and gastric cells.

Comparison of Helicobacter pylori infection between Fukuoka, Japan and Chinju, Korea.

BACKGROUND: Helicobacter pylori is the causative agent of type B chronic gastritis, and plays a major role in the pathogenesis of gastroduodenal ulcer and gastric cancer. Because gastric cancer has been the leading cause of cancer mortality in Japan and Korea, we conducted a seroepidemiological study to estimate the prevalence of H. pylori infection in Japan and Korea in order to explain the current change in the gastric cancer incidences between two countries. MATERIALS AND METHODS: Samples used for this study included 1204 sera from Chinju, Korea and 580 sera from Fukuoka, Japan. Immunoblotting, using a sonicated crude H. pylori antigen and 1:5 dilution of serum, was performed, considering the immunoblot shows reactivity to the 120 Kd antigen of H. pylori as a specific marker of H. pylori infection. RESULTS: Seroepidemiology data from Fukuoka, Japan showed a prevalence of H. pylori infection of 20% before school age, 40% by teenage years, and over 80% beyond 20 years of age. Seroepidemiology data from Chinju, Korea, showed a 50% infection rate in preschool ages, and over 80% prevalence rate after 7 years of age. CONCLUSIONS: Lower rates of childhood H. pylori infection in Fukuoka may explain the recent decline and shift in the incidence of stomach cancer in Japan, supporting the hypothesis that H. pylori is a major determinant in the pathogenesis of stomach cancer.

Increased oxidative DNA damage in Helicobacter pylori-infected human gastric mucosa.

Helicobacter pylori causes type B gastritis. It shows strong association with the development of gastric carcinoma. A plausible hypothesis for the missing link between H. pylori infection and gastric carcinogenesis involves oxygen free radical-induced DNA damage. To test this hypothesis, we compared the amount of 9-hydroxydeoxyguanosine, a marker for oxygen free radical-induced DNA damage, in the DNA of human gastric mucosa with and without H. pylori infection. Gastric antral biopsies were taken from pediatric patients and volunteers to select H. pylori-positive and H. pylori-negative specimens. The 8-hydroxydeoxyguanosine content of the gastric mucosal DNA was measured after H. pylori-positive and H. pylori-negative volunteers were identified. The increased level of oxidative DNA damage suggests the mechanistic link between H. pylori infection and gastric carcinoma.