Contact-dependent cytopathogenic mechanisms of Trichomonas vaginalis

Abstract

The cytopathogenic mechanisms of Trichomonas vaginalis have been debated since the 1940s. We examined the following three proposed pathogenic mechanisms: contact-dependent extracellular killing, cytophagocytosis, and extracellular cytotoxins. Serial observations of Chinese hamster ovary (CHO) cell monolayers exposed to trichomonads revealed that (i) trichomonads form clumps, (ii) the clumps adhere to cells in culture, and (iii) monolayer destruction occurs only in areas of contact with T. vaginalis. Kinetic analysis of target cell killing by trichomonads revealed that the probability of CHO cell death was related to the probability of contact with T. vaginalis, supporting the observation by microscopy that trichomonads kill cells only by direct contact. Simultaneous studies of "lindium oxine label release from CHO cells and trypan blue dye exclusion demonstrated that T. vaginalis kills target cells without phagocytosis. Filtrates of trichomonad cultures or from media in which trichomonads were killing CHO cells had no effect on CHO cell monolayers, indicating that trichomonads do not kill cells by a cell-free or secreted cytotoxin. The microfilament inhibitor cytochalasin D (10 ,ug/ml) inhibited trichomonad killing of CHO cell monolayers by 80% (P < 0.0001). In contrast, the microtubule inhibitor vinblastine (10-6 M) caused only 17% inhibition of trichomonad destruction of CHO cell monolayers (P < 0.020), whereas colchicine (10-6 M) had no effect. T. vaginalis kills target cells by direct contact without phagocytosis. This event requires intact trichomonad microfilament function; microtubule function appears not to be essential.

Vaginal leukocyte characteristics in urogenital trichomoniasis

“…These factors, along with the possibility of functional exhaustion of phagocytes in a heavily contaminated bacterial environment, might also be responsible for the diminished functional capacity of live vaginal leukocytes. Trichomonads, though producing a cytopathogenic effect on various types of cells (1,16,17), did not reduce venous leukocyte viability and functional capacities in vitro (unpublished observation).…”

Iron regulates growth of Trichomonas vaginalis and the expression of immunogenic trichomonad proteins

“…The absolute necessity of iron for growth and multiplication of T. vaginalis and the high iron requirement of this parasite (Gorretl, 1985) may make it impossible to overcome the nutritional immunity imposed by the host, if trichomonads relied only on the interaction of lactoferrin with its trichomonal receptor. The ability of trichomonads to lyse human erythrocytes (Krieger e( ai., 1983;Dailey e( al.. 1990) and HeLa celts and epithelial cells (Aiderete and Pearlman, 1984;Krieger et aL, 1985) has been established. That red blood cells and epithelial cell extracts stimulate growth in iron-limited medium ( Table 5) strongly suggests that intracellular iron sources, such as cytochromes, ferritin, and haemoglobin, are also likely iron sources for the parasite during infection.…”

Trichomonas vaginalis haemolysis: Evidence of functional pores formation on red cell membranes

“…The mechanism of cell damage utilized by T. vaginalis is not yet completely understood. It has been demonstrated that it is contact dependent [2], and the production of proteases that cause detachment of monolayer cells in vitro has been described [3].…”