Helicobacter pylori infection and host immunity in patients with MALT lymphoma.

K Yokota,PhD,a, S Hayashi,MD,b,H Mano,MD,b Y Hirai,MD,b, K Oguma MD,a

aOkayama University Graduate School of Dentistry and Medicine, Okayama, Okayama Japan bJichi Medical School, Yakushiji, Tochigi, Japan

Introduction H. pylori infection induces various humoral and cellular immunities in gastric mucosa. We found heat shock protein 60kDa (hsp60) may be closely associated with pathogenesis in MALT lymphoma. IgG1 antibodies to hsp60 were significantly correlated with antibodies to H. pylori whole cell in patients with MALT lymphoma. CD40-CD40L dependent B cell proliferation and production of IL-4 was induced by cytokine and/or hsp60 stimulations with MALT lymphoma. However in patients with MALT lymphoma the production of the IFN-γ was at the low levels. Aim DNA microarray was performed to study mRNA expression in lymphocytes from patients with MALT lymphoma. Methods PBMCs (1~106 cells/1 ml) from patients and healthy volunteers were cultured in RPMI 1640 with 10% fetal calf serum in flat-bottomed 24-well plates for 1week in a 5% CO2 incubator. And recombinant H. pylori-hsp60 was added to culture at final concentrations of 10mg/ml. mRNA was labeled with biotin and hybridized to cDNA chip (HO2, Mergen Ltd.) for overnight at 30 C. The chip was washed with SSC and scanned by Affimetrix 418. Results The mRNA expressions of HLA-DR, integrin beta7, and granzyme B in patients with MALT lymphoma were increased by hsp60 stimulation. Conclusion: The pathogenicity of H. pylori may involve not only bacterial virulence factor but also host immunity. Studies of infectious immunity will help explain the mechanisms of H. pylori induced gastrodoudenal diseases.

KEY WORDS: Helicobacter pylori, MALT lymphoma, Heat shock protein, Microarray.

For more information, contact

Paper presented at the International Symposium on Predictive Oncology and Intervention Strategies; Paris, France; February 9 - 12, 2002; in the section on Molecular Pathology.