Helicobacter pylori in gastric mucosa-associated lymphoid tissue type lymphoma

Infection with Helicobacter pylori triggers the acquisition of gastric mucosa-associated lymphoid tissue (MALT) and provides the background for MALT-type lymphoma development. This concept has been supported by a high association of H. pylori infection and MALT-type lymphoma and by the regression of most lymphomas after eradication therapy. In almost all patients with MALT-type lymphoma, serum antibodies to H. pylori were detectable. However, H. pylori was found only in 78% of the patients on histological examination. In addition to other effects, changes in the gastric micro-milieu caused by tumor infiltration of the gastric mucosa may be responsible for the loss of the bacterium. The discrepancy of high seroprevalence and lower histological yield has been already described in other gastric diseases, e.g. atrophic gastritis or gastric carcinoma with extensive destruction of the gastric mucosa. H. pylori strains expressing the CagA protein have been associated with duodenal ulceration and gastric carcinoma. A very high percentage of patients with MALT-type lymphoma is also infected by CagA+ strains of H. pylori as tested by immunoblotting. Antibodies directed to CagA were detectable in the serum as well as in micro-cultured gastric mucosa. Infection with H. pylori may be a precondition for the development of gastric MALT-type lymphoma. In particular, CagA+ strains of H. pylori may, together with additional up to now unknown factors, play a role in the development of gastric MALT-type lymphoma.