Molecular basis of host epithelial cell recognition by Trichomonas vaginalis

Abstract

Parasitism of host epithelial cells by Trichomonas vaginalis is a highly specific event. Four trichomonad surface proteins (adhesins) with molecular masses of 65,000 daltons (65 kDa; AP65), 51 kDa (AP51), 33 kDa (AP33), and 23 kDa (AP23) mediate the interaction of T. vaginalis with epithelial cells. Fresh isolates, when compared with long-term-grown isolates, had greater amounts of adhesins, which corresponded with increased levels of cytoadherence. Anti-adhesin antibodies reacted by immunoblot only with the respective protein and detected, by indirect immunofluorescence, each adhesion on the parasite surface. These antibodies inhibited the binding of live parasites to epithelial cells and protected epithelial cells from contact-dependent cytotoxicity. The pretreatment of epithelial cells with a preparation of purified adhesions also blocked trichomonal cytoadherence. Moreover, HeLa cells possessed molecules which recognized and bound to adhesins on nitrocellulose blots.

Characterization of Trichornonas vaginalis AP33 adhesin and cell surface interactive domains

“…The use of HeLa cells in monolayer culture as the in vitro model for cytoadherence studies has been detailed previously (Arroyo & Alderete, 1989;Arroyo et al, 1992Arroyo et al, , 1993. Briefly, HeLa cells were grown to confluence in individual wells ( -8 x lo4 cells) of 96-well plates in Dulbecco's modified Eagle's medium with 10 ' / o foetal bovine serum in 7.5 ' / o CO, atmosphere.…”

“…The fresh clinical T. vaginalis isolate (Arroyo et al, 1992), from which the cDNA library was made, was used for all assays. The trichomonads were grown at 37 "C in Trypticase-yeast extract-maltose (TYM) medium supplemented with 10 ' / o heat-inactivated horse serum (Diamond, 1957).…”

“…Women require drug intervention to eliminate this parasite (Miiller et al, 1980), illustrating an adaptation to survival in the constantly changing environment of the human vagina. Adherence to host vaginal epithelial cells is essential for initiation and maintenance of infection by this mucosal parasite, and four trichomonad surface proteins that mediate parasite cytoadherence to host cells have been identified (Alderete & Garza, 1988;Arroyo et al, 1992).…”

Inducing Immune Protection Against Trichomonas vaginalis: A Novel Vaccine Approach to Prevent HIV Transmission

“…Gene regulation is influenced by contact with epithelial cells (Kucknoor et al, 2005) and cytoadherence has been noted as a better predictor of in vivo pathogenicity than cytotoxicity by soluble factors (Escario et al, 1995). Unfortunately the pathogenic role of adhesion proteins such as AP65, AP51, AP33 and AP23 that have been associated with epithelial cell binding of T. vaginalis (Alderete & Garza, 1984;Arroyo et al, 1992) have not conclusively been elucidated. Midlej & Benchimol (2010) suggests that adherence may aid phagocytic capability and disruption of monolayers in which T. vaginalis literally mechanically disassembles and phagocytoses membranes of epithelial monolayers in vitro similar to previous findings in amoebae and macrophages during ingestion of tumour cells (Chambers & Weiser, 1969, as cited in Midlej & Benchimol, 2010Martinez-Paolmo et al, 1985, as cited in Midlej & Benchimol, 2010.…”

Trichomonas vaginalis: Clinical relevance, pathogenicity and diagnosis

“…The synthesis and transport of these adhesins to the outer membrane occurs in response to the contact of the parasite with vaginal epithelial cells, in tandem with a morphological shift to the amoeboid form. After adherence, the T. vaginalis cells recruit further parasites to the location, forming sizeable aggregates of ameboid cells on the epithelial surface (Arroyo et al, 1992).…”