Trichomonas vaginaliskills and eats – evidence for phagocytic activity as a cytopathic effect

Abstract

This study reports that the cytopathic effect of Trichomonas vaginalis, an important human parasite of the urogenital tract, occurs due to mechanical stress and subsequent phagocytosis of the necrotic cells. The investigation was done using a primary culture of bovine oviduct epithelial cells (BOECs), grown either in monolayers or as floating cells. Trophozoites displaying different virulence levels were co-incubated with BOECs for times varying between 1 min and 48 h. Analyses were performed using videomicroscopy, scanning and transmission electron microscopy, colourimetric assays and cytochemistry. Injury was observed as early as 1 h after incubation, while after 12 h the host cells were severely damaged when a fresh trichomonad isolate was used. Trichomonads attack the host cells by clustering around them. Mechanical stress on the microvilli of the host cells was observed and appeared to induce plasma membrane damage and cell death. After membrane injury and lysis, fragments of the necrotic cells were ingested by trichomonads. Phagocytosis occurred by trichomonads avidly eating large portions of epithelial cells containing the nucleus and other organelles, but living or intact cells were not ingested. Necrotic fragments were rapidly digested in lysosomes, as shown by acid phosphatase and ruthenium red assays where only the BOECs were labelled. The lytic capacity of the trichomonads was more pronounced in host cell suspensions.

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

“…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. Particularly, whole, viable cells are not phagocytosed yet destruction of epithelial cell layers is observed suggesting necrotizing ability of T. vaginalis.…”

Unexplained Infertility Caused by a Latent but Serious Intruder: Trichomonas vaginalis?

“…In 2008, Benchimol et al [9] report that, after one hour of interaction between T. vaginalis and sperm cells in an in-vitro environment, 75% of the sperm cells were immotile or dead. Under scanning electron microscopy, the interaction of T. vaginalis and sperm cells results in high agglutination, membrane protrusions, or channels between the sperm plasma membrane and parasite surface as a mechanism of phagocytosis of T. vaginalis [9,42]. Keeping this in mind, cyto-adhesion and phagocytic activity of trichomonas to ingest and digest spermatozoa in an in-vitro environment suggest a similar behavior in an in-vivo environment as a cause for decreasing numbers of motile sperm directly affecting reproductive success.…”

Comparative aspects of immunity and vaccination in human and bovine trichomoniasis: a review

“…The interactions of Tritrichomonas foetus and Trichomonas vaginalis with host epithelial cells are associated with the activation of different proteases causing epithelial cell apoptosis (Midlej et al 2009;Midlej and Benchimol 2010). In vivo, Tritrichomonas foetus initially adheres to and infects the vagina, causing vaginitis, and then ascends to the uterus and oviduct (Anderson et al 1996;BonDurant et al 2003) and may also cross the placenta.…”