Role for α-L-Fucosidase in the Control of elicobacter pylori-infected Gastric Cancer Cells
Date Issued
2009
Date
2009
Author(s)
Liu, Ta-Wei
Abstract
Infecting about one-half of the global human population, Helicobacter pylori is well established as the primary cause of gastritis, duodenal ulcer and gastric cancer. Currently there is no clear information regarding if and how host cells interact with H. pylori and if such interactions are dependent on the type of gastric disease. Using fluorescently labeled fucose-containing glycoconjugates, we provide the first evidence observing both the uptake of L-fucose from gastric cancer cells to H. pylori and that human α-L-fucosidase 2 (FUCA2) is secreted only under co-culture conditions (i.e., host cells infected with H. pylori). Upon depletion of FUCA2 by RNA interference and detection of translocated CagA (a virulence factor of H. pylori) in host cells, FUCA2 was found to be essential for H. pylori adhesion, in particular to the gastric cancer- and duodenal ulcer-specific strains. Additionally FUCA2 was shown to significantly enhance the expression of Lewis x antigen in H. pylori, which is critical for the bacterial cell adhesion in the pathogenesis and defense strategy to escape from host surveillance. These findings not only demonstrate an important connection between FUCA2 and the adhesion, growth and pathogenicity of H. pylori, but also support the idea that FUCA2 is a potential target for clinical diagnosis and therapeutic intervention of H. pylori-related diseases.
Subjects
Helicobacter pylori
fucose
fucosidase
virulence
gastric disease
SDGs
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