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Background : In spite that several lines of evidence suggest that gastric MALT lymphoma arises from Helicobacter pylori (H. pylori)-associated acquired MALT(mucosa-associated lymphoid tissue), the exact underlying pathogenic mechanism has not yet been clearly exploited. The high expression of B cell...

Background : In spite that several lines of evidence suggest that gastric MALT lymphoma arises from Helicobacter pylori (H. pylori)-associated acquired MALT(mucosa-associated lymphoid tissue), the exact underlying pathogenic mechanism has not yet been clearly exploited. The high expression of B cell attracting chemokine-1 (BCA-1) and modulation of cell death by apoptosis have been suggested as possible pathogenic determinants for whether the cases with H. pylori infection will develop MALToma or not. Methods : We have studied the expression of BCA-1 and its receptor CXCR5 in gastric tissue samples obtained from patients suffering with H. pylori-positive gastritis, H. pylori-negative gastritis and H. pylori-positive low grade MALT lymphoma, respectively. TUNEL (Terminal deoxynucleotidyl Transferase Biotin-dUTP Nick End Labeling) staining for detecting apoptotic cells was also included. Furthermore, the changes of the BCA-1 and CXCR5 expressions before and after the complete remission of MALToma were compared. The in vitro influencing effect of H. pylori infection on the BCA-1 and CXCR5 expression was observed. Results : Significantly higher levels of BCA-1 and its receptor CXCR5 expression were observed in H.pylori-positive MALToma specimens as compared with either the H. pylori-positive gastritis or H. pylori-negative gastritis specimens; its levels were significantly reduced after the remission of MALToma. In contrast to the increased apoptotic activity after H. pylori infection, a significant reduction of epithelial apoptosis was observed in the H. pylori-positive MALToma specimens. H. pylori infection directly induced the expression of BCA-1 in the cultured gastric epithelial cells. Conclusion : The up-regulated BCA-1 expression and the decreased apoptosis in H. pylori infected gastric epithelial cells might contribute to the development of MALT lymphoma.

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