Use of egg yolk-derived immunoglobulin as an alternative to antibiotic treatment for control of Helicobacter pylori infection.

The present study evaluated the potential use of immunoglobulin prepared from the egg yolk of hens immunized with Helicobacter pylori (immunoglobulin Y [IgY]-Hp) in the treatment of H. pylori infections. The purity of our purified IgY-Hp was 91.3%, with a yield of 9.4 mg of IgY per ml of egg yolk. The titer for IgY-Hp was 16 times higher than that for IgY in egg yolk from nonimmunized hens, and IgY-Hp significantly inhibited the growth and urease activity of H. pylori in vitro. Bacterial adhesion on AGS cells was definitely reduced by preincubation of both H. pylori (10(8) CFU/ml) and 10 mg of IgY-Hp/ml. In Mongolian gerbil models, IgY-Hp decreased H. pylori-induced gastric mucosal injury as determined by the degree of lymphocyte and neutrophil infiltration. Therefore, in this experimental model, H. pylori-associated gastritis could be successfully treated by orally administered IgY-Hp. The immunological activity of IgY-Hp stayed active at 60 degrees C for 10 min, suggesting that pasteurization can be applied to sterilize the product. Fortification of food products with this immunoglobulin would significantly decrease the H. pylori infection. In conclusion, the IgY-Hp obtained from hens immunized by H. pylori could provide a novel alternative approach to treatment of H. pylori infection.

Association of the myeloperoxidase -463G-->A polymorphism with development of atrophy in Helicobacter pylori-infected gastritis.

OBJECTIVES: Although the host factors governing clinical outcomes subsequent to Helicobacter pylori infection have not yet been defined, it has been generally perceived that the development of the atrophic gastritis is determined more by host-related factors than by bacterial factors. It is very important to define the host factors controlling the pathway to atrophic gastritis, which is the precursor of gastric cancer. H. pylori infection is characterized by extensive infiltration of neutrophils. Myeloperoxidase in neutrophils amplifies the oxidative potential of hydrogen peroxides that induce gastric mucosal damage, and thus myeloperoxidase is suspected to play a role in H. pylori-induced gastric injury. The aim of this study was to elucidate the association of host myeloperoxidase genetic polymorphism with atrophic gastritis upon H. pylori infection. METHODS: Biopsy specimens taken from the gastric mucosa were examined histologically using the updated Sydney System in 127 Korean patients. The polymerase chain reaction-restriction fragment length polymorphism assay was used to characterize myeloperoxidase genotypes. RESULTS: The distributions of myeloperoxidase genotypes in Korea were 81.9% for myeloperoxidase (G/G) and 18.1% for myeloperoxidase (G/A). No myeloperoxidase (A/A) genotype was observed in 127 patients studied. The degree of active inflammation increased with the increase in H. pylori colonization. A strong positive correlation between the levels of neutrophil infiltration and gastric atrophy was found in the myeloperoxidase (G/G) genotype but not in myeloperoxidase (G/A). CONCLUSIONS: These results suggest that myeloperoxidase genotype is a critical determinant in the pathogenesis of atrophic gastritis subsequent to H. pylori infection. More work is needed to clarify the functional relevance of myeloperoxidase genetic polymorphisms to gastric cell injury.