Lectin Binding Pattern in the Uterus of Pregnant Mice Infected with Tritrichomonas foetus (original) (raw)

Histological and Lectin Binding Changes in the Genital Tract of Mice Infected with Tritrichomonas foetus

Journal of Comparative Pathology, 2008

An experimental murine model of bovine genital tritrichomonosis is described. Female mice were inoculated per vaginam with Tritrichomonas foetus and a sample of the study population was killed every 3 days up to 60 days post-infection. Microscopical changes in the reproductive organs were assessed and immunohistochemistry was used to detectT. foetus within these tissues. Lectin histochemistry was used to determine changes in the expression of carbohydrates within the reproductive mucosa. A range of microscopical changes were detected in the uterine endometrium by 10 days post-inoculation and these were associated with the presence of the protozoan. The endometrial changes included endometritis and ulceration, mucosal atrophy and glandular metaplasia, and were similar to those reported in naturally infected cows. Changes in lectin binding were recognized ¢rst in the vagina where there was increased binding of Ulex europaeus agglutinin-1 (UEA-1) which was maximal on day 16 postinoculation. Within the uterus, there was increased binding of soy bean agglutinin (SBA) which was maximal on day 19 post-inoculation, and of peanut agglutinin (PNA) which was maximal on day 16 post-inoculation. These changes in carbohydrate expression parallel the infection kinetics, since they appeared ¢rst in the vagina and later in the uterus. The changes may re£ect either a host reaction against the infection or the production of enzymes by T. foetus, which act to enhance adhesion and colonization of the genital organs by the organism. The kinetics and pathogenesis of this murine infection are similar to those of the natural bovine disease, suggesting that this model system may be valuable for further studies of this disease. r

Lectin Binding Patterns and Immunohistochemical Antigen Detection in the Genitalia of Tritrichomonas foetus-infected Heifers

Journal of Comparative Pathology, 2004

Heifers inoculated intra-vaginally with Tritrichomonas foetus were examined after long-term infection (70 days) and short-term infection (20 days) by lectin-histochemical, immunohistochemical and cultural techniques. The organism was recovered from the genital tract and T. foetus antigens were detected immunohistochemically in the lumina of uterine glands and cytoplasm of vaginal subepithelial macrophages. An increase of galactosylated residues (galactose and N-acetyl galactose), binding to PNA, was observed in the genital epithelium (vagina, uterus and oviduct) from infected animals. In the oviductal epithelium of short-but not long-term infected heifers, mannose (binding to Con A) was detected, suggesting that the persistent presence of T. foetus and its virulence factors or inflammatory processes result in a change in the glycoproteins of the epithelial surface. The findings have implications for the adhesion of T. foetus to cells and for the pathogenesis of bovine trichomonosis. q

Adhesion of Tritrichomonas foetus to bovine vaginal epithelial cells

Infection and immunity, 1999

An in vitro culture system of bovine vaginal epithelial cells (BVECs) was developed to study the cytopathogenic effects of Tritrichomonas foetus and the role of lipophosphoglycan (LPG)-like cell surface glycoconjugates in adhesion of parasites to host cells. Exposure of BVEC monolayers to T. foetus resulted in extensive damage of monolayers. Host cell disruption was measured quantitatively by a trypan blue exclusion assay and by release of (3)H from [(3)H]thymidine-labeled host cells. Results indicated contact-dependent cytotoxicity of host cells by T. foetus. The cytopathogenic effect was a function of T. foetus density. Metronidazole- or periodate-treated T. foetus showed no damage to BVEC monolayers. A related human trichomonad, Trichomonas vaginalis, showed no cytotoxic effects, indicating species-specific host-parasite interactions. A direct binding assay was developed and used to investigate the role of a major cell surface LPG-like molecule in host-parasite adhesion. The resu...

Interaction of Tritrichomonas foetus and the bovine oviduct in an organ culture model

Veterinary Parasitology, 2006

Tritrichomonas foetus is an extracellular parasite of the reproductive tract in cattle. The mechanism by which T. foetus causes abortion in cattle is largely unknown. There are no studies of infection in the cow oviducts, almost all published papers are related to vagina infection and few articles focusing on the uterus. The aim of the present study was to establish a working model of bovine oviduct epithelial cells and submit these cells to Tritrichomonas foetus interaction. Twenty bovine oviducts were obtained from cows at a commercial abattoir and T. foetus was injected through the isthmus into the oviduct lumen. The whole oviduct was analyzed by scanning and transmission electron microscopy. The results reported here demonstrate that: (1) fresh whole oviducts can be used as a good model to study parasite-host cell interaction; (2) cow oviduct epithelium has been shown to consist of two cell types: ciliated and nonciliated secretory cells, and T. foetus displayed great specificity for the nonciliated cells localized in the deeper oviduct folds; (3) T. foetus adheres as single separate cells, and maintains the flagella externalized; (4) differently from T. vaginalis, T. foetus does not change its shape during the adhesion process; and (5) oviduct cells exhibited morphological characteristics of apoptosis after trichomonadal interaction. #

Tritrichomonas foetus: Experimental infection in pregnant BALB/c mice

Experimental Parasitology, 2008

Bovine genital tritrichomonosis is a venereal disease produced by the flagellate Tritrichomonas foetus. The disease is characterized by the repetition of oestrus and infertility due to embryonic or foetal death. Numerous experimental rodent models have been developed, but none of them has been applied in pregnant females. In this work, we reproduced genital tritrichomonosis in pregnant BALB/c mice. The results were analysed considering the following pregnancy phases: early, middle and final. In the infected group, embryonic loss was significantly higher and occurred in the early and middle phases, in accordance with the time of embryo death in infected bovines. In infected animals at the early phase of pregnancy there was evidence of embryonic death without inflammatory changes in the uterus, suggesting a pathogenic mechanism that does not involve direct tissue damage. In the later days, conceptus loss was associated with endometritis and changes in the decidua.

Experimentally induced intravaginal Tritrichomonas foetus infection in a mouse model

Pesquisa Veterinária Brasileira, 2005

Soto P., Echevarría H.M., Monteavaro C.E. & Catena M.C. 2005. [Experimentally induced Experimentally induced Experimentally induced Experimentally induced Experimentally induced intravaginal intravaginal intravaginal intravaginal intravaginal T T T T Tritrichomonas foetus ritrichomonas foetus ritrichomonas foetus ritrichomonas foetus ritrichomonas foetus infection in a mouse model infection in a mouse model infection in a mouse model infection in a mouse model infection in a mouse model.] Pesquisa Veterinária Brasileira 25(4):225-230. The interest to develop research on the host-parasite relationship in bovine tritrichomonosis has accomplished the use of experimental models alternative to cattle. The BALB/c mouse became the most appropriate species susceptible to vaginal Tritrichomonas foetus infection requiring previous estrogenization.

Study of the Uterine Local Immune Response in a Murine Model of Embryonic Death Due to Tritrichomonas foetus

American Journal of Reproductive Immunology, 2012

Problem Bovine tritrichomonosis is a sexually transmitted disease caused by Tritrichomonas foetus, characterized by conceptus loss. We developed a mouse model of tritrichomonosis to study the mechanisms involved in the embryonic death. We hypothesized that embryonic death may be due to an exacerbated maternal response to the pathogen that then affects embryo development. Method of study We infected BALB/c mice with Tritrichomonas foetus and paired them after confirming active infection. We studied the expression of pro-and anti-inflammatory cytokines, markers for T regulatory and T helper 17 cells as well as haem-oxygenase-1 expression in uterine tissue by realtime RT-PCR. Results As expected, TNF-a was augmented in infected animals. IL-10 and IL-4 were also up-regulated. Treg-associated genes were higher expressed in uteri of infected group. In mice that have lost their conceptus after the infection, haem-oxygenase-1 (HO-1) mRNA levels were strongly decreased, while RORct mRNA, a reliable marker for Th17, was augmented in uterus. Conclusion A T effector response of type 1 and 17 may be involved in tritrichomonosis-related embryonic death. This alters protective mechanisms as HO-1. Increased regulatory T cells may facilitate embryonic death by promoting the persistence of infection.

Trichomonas vaginalisandTritrichomonas foetus:Expression of Chitin at the Cell Surface

Experimental Parasitology, 1998

The expression of chitin as a structural component of Trichomonas vaginalis and Tritrichomonas foetus was demonstrated by using enzymatic hydrolysis by recombinant (rec-) chitinase, chemical analysis, lectin, fluorescent Calcofluor and antibody binding, glycosidases of known specificity, high-performance liquid chromatography (HPLC), and flow cytometry. Chitinous structures were characterized by their insolubility in hot alkali and by releasing Trichomonas vaginalis and Tritrichomonas foetus are flagfrom the decreased reactivity with whole parasites of ligands such ellated protozoan parasites of the urogenital tract of humans as Lycopersicon esculentum (TOL) and Solanum tuberosum lectins, and cattle, respectively. The mechanisms of the infection fluorescent Calcofluor, and anti-chitin antibody, after cell treatment are not well established, although it is possible that the with rec-chitinase. Binding of [ 125 I]TOL showed that, in T. vaginalis interaction of the parasites with the surface of epithelial cells and T. foetus, the numbers of lectin receptors per cell were 4.2 ϫ 10 5 and 3.0 ϫ 10 5 , respectively. Binding of the lectin to the trichomonad could be a factor in the pathogenesis of the disease, which surface was markedly decreased by treatment with rec-chitinase. TOL includes abortion or infertility or both (Honigberg 1978a,b; interaction with the parasites was not affected by N-acetyl-␤-D-gluco-Krieger et al. 1985; Alderete et al. 1995). It is well recogsaminidase treatment, showing that the lectin receptors consisted of ␤nized that glycoconjugates play a major role in cell-cell linked GlcNAc polymers and not of terminal ␤-linked GlcNAc resiinteraction, cell recognition, and cell antigenicity (Hakomori dues.