Signalling of Trichomonas vaginalis for amoeboid transformation and adhesin synthesis follows cytoadherence

Abstract

The cytoadherence of Trichomonas vaginalis, the sexually transmitted flagellated protozoan, to vaginal epithelial cells (VECs) is the key to infection. Electron microscopy revealed that in vitro-grown parasites having typical globular shape transformed rapidly after contact with VECs into thin, flat, amoeboid cells, maximizing the area of adhesion to the surface of VECs. Amoebic trichomonads formed filopodia and pseudopodia, which interdigitated at distinct sites on the plasma membrane of target cells. In contrast, the amoeboid transformation did not occur for T. vaginalis interacting with HeLa cells, the previously used in vitro host model cell. Initial parasitism of VECs by a single organism was followed by establishment of a monolayer of trichomonads on the host cell. Finally, parasites adhering to either VECs or HeLa cells were induced to synthesize greater amounts of the four previously described adhesins. Therefore, distinct signals after contact with either epithelial cell type leads to the morphological transformation and/or induction of adhesion synthesis by T. vaginalis.

Rho GTPases as pathogen targets: Focus on curable sexually transmitted infections

“…93 Actually, the binding to host cells causes the transition of T. vaginalis from an ovoid, free-swimming parasite into an amoeboid, highly adherent form. 94 This process involves a transcriptomic response in the parasite that is triggered by contact with the host cell surface, which increases the expression of genes related to protein synthesis, phenotypic plasticity and host cell degradation. In fact, a major up-regulation of actin and actinassociated genes is evident, suggesting a role for the cytoskeleton in the amoeboid transition.…”

Mechanisms ofTritrichomonas foetusPathogenicity in Cats with Insights from Venereal Trichomonosis

“…Upon initial binding to vaginal epithelial cells, signal transduction events upregulate the transcription of T. vaginalis virulence genes and stimulate trichomonads to undergo a rapid morphological transformation from a pear‐like shape to a flattened amoeboid organism44, 45 (Fig 1C). During this transformation, trichomonads extend short filopodia toward epithelial cells and numerous membrane–membrane contact points can be observed 45. Amoeboid transformation likely maximizes host cell contact, which is essential for effective adherence in the challenging, secretory environment of the vagina.…”

“…Under iron‐rich conditions and upon contact with epithelial cells, trichomonads express and mobilize adhesin proteins to their cell surface 45, 55. At least one bovine T. foetus and five functionally diverse T. vaginalis adhesin proteins, named on the basis of their molecular weights ( T. foetus : Tf190; T. vaginalis : AP120, AP65, AP51, AP33, AP23) have been identified 48, 49, 56, 57.…”

Human Trichomoniasis due to Trichomonas vaginalis - Current Perspectives

“…Initially, following cytoadherence, parasite changes its morphology from pear shape to amoeboid form with numerous cytoplasmic projections interdigetating with the microvilli of the host cell plasma membrane (Arroya et al, 1993) and allowing the formation of isolated intracelllular spaces (Gonzalez et al, 1995). The adherence is specifically mediated by four adhesion proteins (AP 65,51,33 and 23) which act in a specific receptor-ligand interaction and is time, temperature and pH dependent.…”