scholarly journals Trichomonas vaginalis: current understanding of host–parasite interactions

2011 ◽  
Vol 51 ◽  
pp. 161-175 ◽  
Author(s):  
Christopher M. Ryan ◽  
Natalia de Miguel ◽  
Patricia J. Johnson
Keyword(s):  
Drug Targets ◽  
Trichomonas Vaginalis ◽  
Molecular Data ◽  
Host Cells ◽  
Current Status ◽  
Rational Approach ◽  
Sexually Transmitted ◽  
Host Parasite Interactions ◽  
Future Challenges ◽  
Host Parasite

Trichomonas vaginalis is a sexually transmitted obligate extracellular parasite that colonizes the human urogenital tract. Despite being of critical importance to the parasite's survival relatively little is known about the mechanisms employed by T. vaginalis to establish an infection and thrive within its host. Several studies have focused on the interaction of the parasite with host cells and extracellular matrix, identifying multiple suspected T. vaginalis adhesins. However, with the exception of its surface lipophosphoglycan, the evidence supporting a role in adhesion is indirect or controversial for many candidate molecules. The availability of the T. vaginalis genome sequence paved the way for genomic analyses to search for proteins possibly involved in host–parasite interactions. Several proteomic analyses have also provided insight into surface, soluble and secreted proteins that may be involved in Trichomonas pathogenesis. Although the accumulation of molecular data allows for a more rational approach towards identifying drug targets and vaccine candidates for this medically important parasite, a continued effort is required to advance our understanding of its biology. In the present chapter, we review the current status of research aimed at understanding T. vaginalis pathogenesis. Applied experimental approaches, an overview of significant conclusions drawn from this research and future challenges are discussed.

scholarly journals 895 Trichomonas vaginalis exosomes deliver cargo to host cells and mediate host: Parasite interactions

2018 ◽  
Vol 138 (5) ◽  
pp. S152
Author(s):  
O. Twu ◽  
N. de Miguel ◽  
G. Lustig ◽  
G. Stevens ◽  
A. Vashishit ◽  
...  
Keyword(s):  
Trichomonas Vaginalis ◽  
Host Cells ◽  
Host Parasite Interactions ◽  
Host Parasite

scholarly journals Trichomonas vaginalis Exosomes Deliver Cargo to Host Cells and Mediate Host∶Parasite Interactions

2013 ◽  
Vol 9 (7) ◽  
pp. e1003482 ◽  
Author(s):  
Olivia Twu ◽  
Natalia de Miguel ◽  
Gila Lustig ◽  
Grant C. Stevens ◽  
Ajay A. Vashisht ◽  
...  
Keyword(s):  
Trichomonas Vaginalis ◽  
Host Cells ◽  
Host Parasite Interactions ◽  
Host Parasite

The Role of Purinergic Signaling in Trichomonas vaginalis Infection

2020 ◽  
Vol 20 ◽  
Author(s):  
Micheli Ferla ◽  
Tiana Tasca
Keyword(s):  
Drug Targets ◽  
Trichomonas Vaginalis ◽  
Hiv Transmission ◽  
Cell Damage ◽  
Purinergic Signaling ◽  
Host Cells ◽  
Purine Nucleotides ◽  
Cellular Effects ◽  
Adverse Pregnancy ◽  
Purine Salvage Pathways

: Trichomoniasis, one of the most common non-viral sexually transmitted infections worldwide, is caused by the parasite Trichomonas vaginalis. The pathogen colonizes the human urogenital tract and the infection is associated with complications such as adverse pregnancy outcomes, cervical cancer, and an increase in HIV transmission. The mecha-nisms of pathogenicity are multifactorial, and controlling immune responses is essential for infection maintenance. Extra-cellular purine nucleotides are released by cells in physiological and pathological conditions, and they are hydrolyzed by enzymes called ecto-nucleotidases. The cellular effects of nucleotides and nucleosides occur via binding to purinoceptors, or throughthe uptake by nucleoside transporters. Altogether, enzymes, receptors and transporters constitute the purinergic signaling, a cellular network that regulates several effects in practically all systems including mammals, helminths, proto-zoa, bacteria, and fungi. In this context, this review updates the data on purinergic signaling involved in T. vaginalis biol-ogy and interaction with host cells, focusing on the characterization of ecto-nucleotidases and on purine salvage pathways. The implications of the final products, the nucleosides adenosine and guanosine, for human neutrophil response and vagi-nal epithelial cell damage reveal the purinergic signaling as a potential new mechanism for alternative drug targets.

scholarly journals BspA and Pmp proteins ofTrichomonas vaginalismediate adherence to host cells

2018 ◽  
Author(s):  
Maria R. Handrich ◽  
Sriram G. Garg ◽  
Ewen W. Sommerville ◽  
Robert P. Hirt ◽  
Sven B. Gould
Keyword(s):  
Trichomonas Vaginalis ◽  
Functional Characterization ◽  
Surface Proteins ◽  
Host Cells ◽  
Protein Families ◽  
Sexually Transmitted ◽  
Trace Back ◽  
Oral Pathogens ◽  
Adhesion Performance

AbstractTrichomonas vaginalisis one of the most widespread, sexually transmitted pathogens. The infection involves a morphological switch from a free-swimming pyriform trophozoite to an amoeboid cell upon adhesion to host epithelial cells. While details on how the switch is induced and to what proteins of the host surface the parasite adheres remain poorly characterized, several surface proteins of the parasite itself have been identified as potential candidates. Among those are two expanded protein families that harbor domains that share similarity to functionally investigated surface proteins of prokaryotic oral pathogens; these are the BspA proteins of Bacteroidales and Spirochaetales, and the Pmp proteins of Chlamydiales. We sequenced the transcriptomes of five Trichomonads and screened for the presence of BspA and Pmp domain-containing proteins and tested the ability of individualT. vaginaliscandidates to mediate adhesion. Here we demonstrate that (i) BspA and Pmp domain-containing proteins are specifically expanded inT. vaginalisin comparison to other Trichomonads, and that (ii) individual proteins of both families have the ability to increase adhesion performance in a non-virulentT. vaginalisstrain andTetratrichomonas gallinarum, a parasite usually known to infect birds but not humans. Our results initiate the functional characterization of these two broadly distributed protein families, whose origin we trace back to the origin of Trichomonads themselves.

scholarly journals Critical aspects of phytoalexins in potato

1987 ◽  
Vol 59 (3) ◽  
pp. 217-230
Author(s):  
Sture Brishammer
Keyword(s):  
Host Cells ◽  
Potato Tubers ◽  
Inhibitory Effects ◽  
Host Parasite Interactions ◽  
Different Types ◽  
Endogenous Elicitor ◽  
Artificial Inoculations ◽  
Host Parasite ◽  
Critical Aspects

Phytoalexins in potato are sesquiterpenoid substances produced in response to infections and are believed to help plants resist attack by pathogens. However, these compounds appear in response to compatible as well as incompatible interactions and only accumulate in the tubers. The amounts of phytoalexins produced depend on the physiological condition of the tubers. Young tubers don’t get easily infected with Phytophthora infestans even though they synthesize extremely small amounts of phytoalexins. Furthermore, confusion as to the identity of specific races and the propensity for a given race to produce different effects in the same type of host makes it extremely difficult to predict host-parasite interactions with any acceptable degree of accuracy. It is doubtful that the production of phytoalexins in response to artificial inoculations is representative of that occurring in natural infections. Markedly different types of pathogens induce synthesis of same substances in the host cells. It therefore seems most probable that all the phytoalexins are synthesized in response to stimulation by an endogenous elicitor. Little knowledge is available regarding the biosynthesis of these sesquiterpenes, and many previous determinations have presumably been erroneous. When potato tubers were inoculated with the late blight fungus, secondarily appearing bacteria were not retarded, despite the presence of phytoalexins. There is no generally accepted hypothesis describing the mechanism by which phytoalexins inhibit pathogens and no distinction has been made between the effects on necrotrophs and biotrophs. Adequate bioassays capable of measuring the effects of inhibition have yet to be developed, thus far, no convincing inhibitory effects have been reported. During purification of the phytoalexins there is a high risk for artifact forming, implying that specific compounds cannot be detected with certainty. Moreover, present analytical methods must be improved before we can determine how phytoalexins act in vivo. Probably, phytoalexins are synthesized at a stage in the infection too late to be able to restrict its expansion with the tissues of the host. Phytoalexins are restricted to the attacked parts of the tubers and there is no evidence indicating that these compounds pose any health risks when present in potatoes used for consumption.

scholarly journals A Novel Trichomonas vaginalis Surface Protein Modulates Parasite Attachment via Protein:Host Cell Proteoglycan Interaction

mBio ◽  
2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Brenda M. Molgora ◽  
Anand Kumar Rai ◽  
Michael J. Sweredoski ◽  
Annie Moradian ◽  
Sonja Hess ◽  
...  
Keyword(s):  
Host Cell ◽  
Trichomonas Vaginalis ◽  
Surface Protein ◽  
Host Cells ◽  
Parasite Line ◽  
Cell Adherence ◽  
Common Component ◽  
Content Type ◽  
Sexually Transmitted ◽  
Significant Difference

ABSTRACT Trichomonas vaginalis is a highly prevalent, sexually transmitted parasite which adheres to mucosal epithelial cells to colonize the human urogenital tract. Despite adherence being crucial for this extracellular parasite to thrive within the host, relatively little is known about the mechanisms or key molecules involved in this process. Here, we have identified and characterized a T. vaginalis hypothetical protein, TVAG_157210 (TvAD1), as a surface protein that plays an integral role in parasite adherence to the host. Quantitative proteomics revealed TvAD1 to be ∼4-fold more abundant in parasites selected for increased adherence (MA parasites) than the isogenic parental (P) parasite line. De novo modeling suggested that TvAD1 binds N-acetylglucosamine (GlcNAc), a sugar comprising host glycosaminoglycans (GAGs). Adherence assays utilizing GAG-deficient cell lines determined that host GAGs, primarily heparan sulfate (HS), mediate adherence of MA parasites to host cells. TvAD1 knockout (KO) parasites, generated using CRISPR-Cas9, were found to be significantly reduced in host cell adherence, a phenotype that is rescued by overexpression of TvAD1 in KO parasites. In contrast, there was no significant difference in parasite adherence to GAG-deficient lines by KO parasites compared with wild-type, which is contrary to that observed for KO parasites overexpressing TvAD1. Isothermal titration calorimetric (ITC) analysis showed that TvAD1 binds to HS, indicating that TvAD1 mediates host cell adherence via HS interaction. In addition to characterizing the role of TvAD1 in parasite adherence, these studies reveal a role for host GAG molecules in T. vaginalis adherence. IMPORTANCE The ability of the sexually transmitted parasite Trichomonas vaginalis to adhere to its human host is critical for establishing and maintaining an infection. Yet how parasites adhere to host cells is poorly understood. In this study, we employed a novel adherence selection method to identify proteins involved in parasite adherence to the host. This method led to the identification of a protein, with no previously known function, that is more abundant in parasites with increased capacity to bind host cells. Bioinformatic modeling and biochemical analyses revealed that this protein binds a common component on the host cell surface proteoglycans. Subsequent creation of parasites that lack this protein directly demonstrated that the protein mediates parasite adherence via an interaction with host cell proteoglycans. These findings both demonstrate a role for this protein in T. vaginalis adherence to the host and shed light on host cell molecules that participate in parasite colonization.

scholarly journals Expanding the antimalarial toolkit: Targeting host–parasite interactions

2016 ◽  
Vol 213 (2) ◽  
pp. 143-153 ◽  
Author(s):  
Jean Langhorne ◽  
Patrick E. Duffy
Keyword(s):  
First Generation ◽  
Host Cells ◽  
Mammalian Host ◽  
Drug Resistant ◽  
Intracellular Growth ◽  
Partial Protection ◽  
Anopheles Mosquitoes ◽  
Host Parasite Interactions ◽  
New Research ◽  
Host Parasite

Recent successes in malaria control are threatened by drug-resistant Plasmodium parasites and insecticide-resistant Anopheles mosquitoes, and first generation vaccines offer only partial protection. New research approaches have highlighted host as well as parasite molecules or pathways that could be targeted for interventions. In this study, we discuss host–parasite interactions at the different stages of the Plasmodium life cycle within the mammalian host and the potential for therapeutics that prevent parasite migration, invasion, intracellular growth, or egress from host cells, as well as parasite-induced pathology.

scholarly journals Adhesion of Tritrichomonas foetus to Bovine Vaginal Epithelial Cells

1999 ◽  
Vol 67 (8) ◽  
pp. 3847-3854 ◽  
Author(s):  
B. N. Singh ◽  
J. J. Lucas ◽  
D. H. Beach ◽  
S. T. Shin ◽  
R. O. Gilbert
Keyword(s):  
Epithelial Cells ◽  
Cell Surface ◽  
Trichomonas Vaginalis ◽  
Host Cells ◽  
Tritrichomonas Foetus ◽  
Trypan Blue Exclusion ◽  
Vaginal Epithelial Cells ◽  
Host Parasite

ABSTRACT An in vitro culture system of bovine vaginal epithelial cells (BVECs) was developed to study the cytopathogenic effects ofTritrichomonas foetus and the role of lipophosphoglycan (LPG)-like cell surface glycoconjugates in adhesion of parasites to host cells. Exposure of BVEC monolayers to T. foetusresulted in extensive damage of monolayers. Host cell disruption was measured quantitatively by a trypan blue exclusion assay and by release of 3H from [3H]thymidine-labeled host cells. Results indicated contact-dependent cytotoxicity of host cells byT. foetus. The cytopathogenic effect was a function ofT. foetus density. Metronidazole- or periodate-treatedT. 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 results of competition experiments showed that the binding to BVECs was displaceable, was saturable, and yielded a typical binding curve, suggesting that specific receptor-ligand interactions mediate the attachment of T. foetus to BVECs. Progesterone-treated BVECs showed enhanced parasite binding. T. foetus LPG inhibited the binding of T. foetus to BVECs; the LPG from T. vaginalis and a variety of other glycoconjugates did not. These data imply specificity of LPG on host-parasite adhesion. Periodate-treated parasites showed no adherence to host cells, indicating the involvement of carbohydrate containing molecules in the adhesion process.

Sign in / Sign up

Export Citation Format

Share Document