Phagocytosis by Trichomonas vaginalis: new insights

Abstract

Background information. The parasitic protozoan Trichomonas vaginalis is the causative agent of trichomoniasis, a sexually transmitted disease. The phagocytic activity of this parasite has not been completely elucidated. In order to better understand the mechanisms of trichomonal phagocytosis, we have studied the in vitro capacity of T. vaginalis to phagocytose and degrade Saccharomyces cerevisiae cells. Results and conclusions.To analyse the phagocytic ability and capacity, two isolates of T. vaginalis presenting different virulence grades were used. Complementary techniques, such as fluorescence microscopy, computerbased fluorescence analysis, scanning and transmission electron microscopy and the use of drugs that interfere with the actin microfilaments, were used in order to follow the behaviour of the actin cytoskeleton during phagocytosis of yeast cells by T. vaginalis. It was concluded that: (1) T. vaginalis changes its shape rapidly and engulfs the yeast cells, which are almost as large as the parasite; (2) long-term and fresh cultures are able to phagocytose, although the low-virulence strain JT demonstrated a lower activity when compared with the highly virulent T016 isolate; (3) the T016 strain exhibited an amoeboid morphology during the internalization of yeast cells in contrast with the JT strain; (4) attachment of yeast cells to the parasite occurs via the whole cell surface, including both anterior and recurrent flagella; (5) two forms of phagocytosis were observed: a 'sinking' process without any apparent participation of plasma membrane extensions and the classical phagocytosis where pseudopodia are extended toward the target cell; (6) the internalized S. cerevisiae are digested in lysosomes; (7) competitor sugars D-mannose or L-fucose inhibit the phagocytosis, and inhibition was 1.67 times higher in long-term cultured JT than that of the parasites from fresh isolate T016; (8) a thick layer of actin microfilaments was present underlying the plasma membrane, and especially in the pseudopodia and around the phagocytosed particles; (9) a dramatic change in the distribution pattern of fibrillar actin occurred during phagocytosis; (10) cytochalasin D depressed the phagocytosis; (11) a non-specific recognition and phagocytosis of yeast cells by T. vaginalis is mediated by a mannose receptor present on the parasite surface; (12) the phagocytic process may occur simultaneously during mitosis of the parasite.

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

“…Recently, trichomonas have been isolated from fallopian tubes, peritoneal fluid, and the pouch Douglas, suggesting that motile trichomonas may be able to invade the whole genital tract [32,33]. There are several studies that conclude that T. vaginalis causes urogenital damage to different types of cells and tissues, such as connective and muscular tissues, due to an excessive cytotoxic local effect suggesting high risk of reproductive failure [9,[33][34][35][36][37][38][39]. Trichomonas bind to the cells inducing membrane retraction, cell blebbing, and apoptosis.…”

Trichomonas vaginalis: Clinical relevance, pathogenicity and diagnosis

“…This group of 4 cysteine proteases are also linked to adhesion and the passage of the parasite through the mucosal barrier, making them important factors in T. vaginalis pathogenesis. T. vaginalis is also capable of the in vitro phagocytosis of vaginal epithelial cells, leukocytes and erythroyctes, along with commensal bacteria (Rendon-Maldonado et al, 1998) and yeasts (Pereira-Neves and Benchimol, 2007) of the genital tract. Two distinct mechanisms of phagocytosis have been observed during in vitro studies with yeasts; a classic form of phagocytosis involving extension of pseudopodia, which then engulf the target cell, and also a more passive form, where the target cell sinks into the T.…”

“…vaginalis cells recognise target cells appropriate for phagocytosis is poorly understood, although non-specific mannose receptors on the T. vaginalis outer membrane have been implicated in the internalisation of yeast cells (Pereira-Neves and Benchimol, 2007). Mannose binding lectins have been shown to bind Gram positive and Gram negative bacteria, as well as yeasts, protozoa and even some viruses (Klein and Kilpatrick, 2004), showing the wide range of organisms identifiable by the presence of this ligand.…”

“…vaginalis membrane (Pereira-Neves and Benchimol, 2007). Phagocytosis is followed by intracellular killing in lysosomes, and provides the T. vaginalis cell with a source of nutrients (Francioli et al, 1983).…”

First Report of Feline Intestinal Trichomoniasis Caused byTritrichomonas foetusin Korea

“…After the culture was stabilized, 3 consecutive series of limiting dilution was performed to establish a homogenous isolate. Scanning electron microscopy was used to morphologically identify the organism according to a previously described method by Pereira-Neves and Benchimol [16]. Briefly, culture samples were allowed to adhere on to a cover glass coated with poly L-lysine (Iwaki, Tokyo, Japan) and were fixed in 2.5% glutaraldehyde in 0.1 M cacodylate buffer (pH 7.2) for 2 hr at room temperature.…”