Biliary Migration, Colonization, and Pathogenesis of Co-Infected with .

Co-infection with the A strain of exacerbates the pathology of human liver fluke (OV) infection leading to cholangiocarcinoma. However, underlying mechanisms remain unclear. We report a significant increase in A-positive and A-negative in the stomach, blood, bile, and in the OV worms of co-infected Syrian golden hamsters at one hour, three hours, and one month, post-infection, compared to hamsters infected with either OV or alone. Except in the worms, numbers declined at three months post-infection, particularly in the bile fluid of co-infected animals. Both strains of were immunohistochemically detected in the tegument of the worm, as well as in the bile duct epithelium when co-infected with but not in infection alone. Interestingly, only the A-positive strain was detected in the gut of the worm. Co-infection between A-positive and resulted in a more severe biliary pathology and decreased E-cadherin expression in vivo and in vitro than those of the A-negative strain. These data suggest that acts as a carrier of A-positive and co-migrates to the bile ducts, whereas facilitates colonization and enhances the biliary pathogenesis and carcinogenesis.