Yasuhiro Koga

Prevention of Helicobacter pylori infection by lactobacilli in a gnotobiotic murine model.

BACKGROUND: Helicobacter pylori is a bacterium which causes gastric inflammatory diseases. Oral inoculation of H pylori usually results in only a temporary colonisation without a successful infection in the stomach of conventional mice in which lactobacilli are the predominant indigenous bacteria. AIM: To determine whether lactobacilli exert an inhibitory effect on colonisation by H pylori in the stomach. METHODS: The effects of H pylori on attachment to murine and human gastric epithelial cells and the H pylori mediated release of interleukin-8 (IL-8) by these cells were examined in vitro. Lactobacillus salivarius infected gnotobiotic BALB/c mice and control germ free mice were inoculated orally with H pylori to examine whether L salivarius can inhibit colonisation by H pylori. RESULTS: L salivarius inhibited both the attachment and IL-8 release in vitro. H pylori could not colonise the stomach of L salivarius infected gnotobiotic BALB/c mice, but colonised in large numbers and subsequently caused active gastritis in germ free mice. In addition, L salivarius given after H pylori implantation could eliminate colonisation by H pylori. CONCLUSION: These findings suggest the possibility of lactobacilli being used as probiotic agents against H pylori.

The therapeutic effect of bovine lactoferrin in the host infected with Helicobacter pylori

BACKGROUNDnIt remains unclarified whether bovine lactoferrin (bLF) can exert a therapeutic effect on the host infected with Helicobacter pylori.nnnMETHODSnGermfree BALB/c mice were orally inoculated with H. pylori to induce infection. Three weeks after infection the mice were given bLF orally once daily for 2 or 4 weeks and were then killed to examine the bacterial number in the stomach and the serum antibody titer to H. pylori. To count the number of epithelium-bound H. pylori, the resected stomach was agitated in phosphate-buffered saline to remove non-bound H. pylori before bacterial enumeration.nnnRESULTSnThe administration of 10 mg bLF for 3 to 4 weeks decreased the number of H. pylori in the stomach to one-tenth and also exerted a significant inhibitory effect on the attachment of H. pylori to the stomach. As a result, the serum antibody titer to H. pylori, whose level is presumed to represent the size of the immune response by the host, thereby reflecting the degree of bacterial attack, decreased to an undetectable level.nnnCONCLUSIONSnThese findings suggest that bLF exerts an inhibitory effect on colonizing H. pylori by detaching the bacterium from the gastric epithelium and by exerting a direct anti-bacterial effect.

Helicobacter pylori induces apoptosis in gastric epithelial cells through inducible nitric oxide

Background : Gastric mucosal injury by Helicobacter pylori has been suggested to be mediated by various cytokines induced by this organism. Nitric oxide (NO) is an important effector molecule involved in immune regulation and defence. To clarify the mechanisms by which H. pylori induces gastric mucosal cell injury, we examined whether H. pylori induces gastric epithelial death via NO production.

Flagellin Gene Diversity among Helicobacter pylori Strains and IL-8 Secretion from Gastric Epithelial Cells

BACKGROUNDnTo clarify the pathological functions of the virulence factors of Helicobacter pylori, a comparative analysis was carried out on the relationship between motility, flagellar gene polymorphism, vacuolating cytotoxin (VT) production and interleukin-8 (IL-8) induction.nnnMETHODSnTwenty-five strains were examined for restriction fragment length polymorphism (RFLP) of the flagellin gene. Motility was measured using semisolid agar plates. Cytotoxicity was assayed using RK-13 cells. IL-8 secretion was assessed by the enzyme-linked immunosorbent assay (ELISA) methods.nnnRESULTSnH. pylori was classified into four groups according to their flagellar RFLP. No differences were noted in motility or VT production among the four groups, but a significant difference was noted in IL-8 induction. In addition, highly motile strains produced more IL-8.nnnCONCLUSIONnThis flagellar genetic polymorphism may be associated with IL-8 induction.