Role for α-L-fucosidase in the control of Helicobacter pylori-infected gastric cancer cells

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 depend...

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Bibliographic Details
Published in:Proceedings of the National Academy of Sciences - PNAS 2009, Vol.106 (34), p.14581-14586
Main Authors: Liu, Ta-Wei, Ho, Ching-Wen, Huang, Hsin-Hung, Chang, Sue-Ming, Popat, Shide D, Wang, Yi-Ting, Wu, Ming-Shiang, Chen, Yu-Ju, Lin, Chun-Hung
Format: Article
Language:English
Subjects:
adhesion
alpha-L-fucosidase
antigens
bacteria
cell adhesion
coculture
duodenal ulcers
fucose
gastritis
glycoconjugates
Helicobacter pylori
humans
monitoring
neoplasm cells
pathogenesis
RNA interference
stomach neoplasms
virulence
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Summary: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 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 coculture 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 bacterial cell adhesion in the pathogenesis and defense strategy to escape 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.
ISSN:0027-8424
1091-6490