Host-parasite interactions between Trichomonas vaginalis and human vaginal epithelial cells


Identification: Tai, Jung Hsiang


Description

Host-parasite interactions between Trichomonas vaginalis and human vaginal epithelial cells
 
Yen-Yu Yang1, Hong-Ming Hsu1,2, Yu-Hsin Huang, Tin-Ray Tu1, Daniel Hsu1, Huan-Yuan Chen1, Fu-Tong Liu1, and Jung-Hsiang Tai1,2
1Division of Infectious Diseases and Immunology, Institute of Biomedical Sciences, Academia Sinica, 2Department of Parasitology, College of Medicine, National Taiwan University, Taipei; Taiwan  
 
Cytoadherence of Trichomonas vaginalis onto human epithelial cells from genital tract was previously shown to involve surface glycan and several reputed adhesins. In this study, parasite infection was monitored firstly by a conventional binding assay. A biphasic binding of adherent trophozoites to human vaginal epithelial cells, but not Hela cells, was observed, with an immediate initial phase and a second phase, which could be completed by galactose. Secretion of galectin-1 and -3 was detected at levels higher in spent medium recovered from vaginal epithelial than Hela cell cultures before or after infection. Surface expression of the galactins was only detected on vaginal epithelial cells postinfection. Adherent trophozoites were found in real-time imaging to migrate slowly over short distances exploring neighboring host cells, with some anchored-on host cells via axostyle, while non-adherent trophozoites moved rapidly over host cells. As revealed by the scanning electron microscopy, adherent trophozoites were found to transform from original oval form to roundup form, but the flat amoeba form was less common. Protein acetylation was detected on the recurrent flagellum at a level much higher in trophozoites from adherent than nonadherent isolate. Right after incubation of adherent trophozoites in spent medium, deacetylation of the recurrent flagellum was observed. Acetylation of proteins on apical surface of human vaginal epithelial cells was detected, yet acetylated proteins migrated to the host-parasite junctions right after infection. These observations suggest that adherent parasite may sense host environment and anchor on host cells via axostyle to initiate infection.
 

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