Regulation of host responses by a bacterial peptide
ribosomal protein fragment may contribute to lymphocyte dysfunction in gastric adenocarcinoma.
Helicobacter pylori causes chronic gastritis and can promote the development of gastric adenocarcinoma through mechanisms that remain elusive. In October 15 Journal of Clinical Investigation, Åsa Betten and colleagues from University of Göteborg show that Hp(2-20), a cleaved fragment of an H. pylori ribosomal protein, acts directly on the host immune system, and may contribute to lymphocyte dysfunction in gastric adenocarcinoma.
Betten et al. showed that Hp(2–20), acting via two chemoattractant receptors, attracts and activates monocytes to generate oxygen radicals. These activated monocytes suppressed NK cell and T cell function and triggered apoptosis in both cell types — effects mediated by oxygen radicals. In addition, they found that histamine, a gastric mucosal constituent, protected NK cells/T cells from monocyte-induced functional inhibition and apoptosis (J Clin Invest 2001, 108:1221-1228).
These results may show the missing link between H. pylori and gastric tumors, and the authors suggest that histamine...
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