Host-pathogen interaction between Helicobacter pylori and biliary cells mediated by sialic acid receptor
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Abstract
Commensalism involving H. pylori and O. viverrini may have evolved and may facilitate conveyance of the bacillus into human bile duct. The adherence between bacterial ligands and host receptor is an initial step in colonization of H. pylori in bile duct epithelium leading to disease pathogenesis. We investigated tissue adhesion of FITC-labelled H. pylori on normal, pre-cancerous and cancerous bile duct epithelium from 42 cholangiocarcinoma (CCA) cases. The results revealed that all cases exhibited different degrees of the bacterial adhesion. Quantitatively, normal and pre-cancerous bile duct epithelium showed significantly higher number of H. pylori adhesion per area than those of CCA tissue (p-value < 0.001). The mechanism by which H. pylori binds to the bile duct epithelium was then explored. A H. pylori adhesin, specifically sialic acid-binding adhesin (SabA) which recognizes sialyl-Lewis X glycan receptor was studied in human normal cholangiocytes (H69 cell line). The results revealed that the number of FITC-labelled H. pylori adhesion was significantly decreased after blocking with wheat germ agglutinin (WGA) which binds to sialic acid (p-value < 0.05) but not with
Ulex eropaeus agglutinin I (UEA I) which is specific for alpha-L-fucose. Pretreatment of H69 cells with antibody to sialyl-Lewis X resulted in significantly decreased adhesion of H. pylori-in a dose dependent manner, particularly at a dilution of 1:200 (p-value < 0.005) and 1:1000 (p-value < 0.05). The results clearly show that H. pylori can colonize on the bile duct epithelium and sialyl-Lewis X may be a receptor for the adhesion.
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