The contribution of BCA-1 and apoptosis in gastric MALT lymphoma generation.
- Author:
Choong Keun CHA
1
;
Soojin PARK
;
Yeong Bae KIM
;
Kee Myung LEE
;
Sung Won CHO
;
Ki Baik HAHM
Author Information
1. Department of Gastroenterology and Genomic Research Center for Gastroenterology, Ajou University School of Medicine, Suwon, Korea.
- Publication Type:In Vitro ; Original Article
- Keywords:
Chemokine;
BCA-1;
CXCR5;
Apoptosis;
MALT lymphoma;
Helicobacter pylori
- MeSH:
Apoptosis*;
Cell Death;
DNA Nucleotidylexotransferase;
Epithelial Cells;
Gastritis;
Helicobacter pylori;
Humans;
In Situ Nick-End Labeling;
Lymphoma, B-Cell, Marginal Zone*
- From:Korean Journal of Medicine
2007;72(2):138-150
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
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.
