The effect of the immune response to Helicobacter pylori in the development of intestinal metaplasia.

AIM

To determine whether cytotoxic Helicobacter pylori antibodies occur in gastric mucosa, and whether these antibodies contribute to the development of intestinal metaplasia.

MATERIALS AND METHODS

The number of mononuclear inflammatory cells, which specifically produce immunoglobulin (Ig)G and IgA antibodies, was investigated by using an enzyme-linked immunospot assay and the fraction of mononuclear inflammatory cells determined in gastric biopsy specimens from 34 subjects with H. pylori infection. Assays for the cytotoxicity of H. pylori antibodies were performed on cultured Japanese green monkey kidney (Vero) cells and by in vitro tests.

RESULTS

The number of IgG and IgA antibody-producing cells was positively correlated with the degree of inflammation of the gastric mucosa. However, the number of IgG antibody-producing cells was lower in subjects with intestinal metaplasia than in those without. This was not the case for IgA. Significant cytotoxic damage was observed in Vero cells in vitro when incubated in a solution containing the H. pylori IgG antibody, antigen and polymorphonuclear leukocytes. No cytotoxicity was seen with the IgA antibody or with the antigen or polymorphonuclear leukocytes alone.

CONCLUSIONS

H. pylori infection is associated with the appearance of immunocompetent mononuclear cells in gastric mucosa. These cells produce H. pylori antibodies of the IgG class which are capable of causing cytotoxic damage in the epithelial cells, obviously through activation of polymorphonuclear leukocytes by antibody-antigen complexes. The occurrence of these cells is inversely related to intestinal metaplasia, suggesting that they may be involved in the processes of epithelial damage leading to the appearance of intestinal metaplasia.