ArticleThe Journal of biological chemistry2016
Trichomonas vaginalis Lipophosphoglycan Exploits Binding to Galectin-1 and -3 to Modulate Epithelial Immunity.
Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
36 citing papers in PubMed, 73 citations in OpenAlex.
- Galectin-Levels Are Elevated in Infants Born Preterm Due to Amniotic Infection and Rapidly Decline in the Neonatal Period.Frontiers in immunology · 2020Trial
- Impact of pH andProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Trichomonas vaginalis Drug Targets and Their Role in Drug Discovery and Development.Pharmaceutical research · 2026Review
- Recent Advances in Biology, Host and Microbe Interactions of the Human Sexually Transmitted ParasiteInternational journal of molecular sciences · 2025Review
- Perineal Urethrostomy Enables Susceptibility of Bull Calves as a Natural Host Model for Bovine Trichomonosis.Microorganisms · 2025Article
- Iron triggersmBio · 2025Article
- Investigation ofInternational journal of molecular sciences · 2024Article
- Resident microbes shape the vaginal epithelial glycan landscape.Science translational medicine · 2023Article
- Review
- The interaction between adhesion protein 33 (TvAP33) and BNIP3 mediates the adhesion and pathogenicity of Trichomonas vaginalis to host cells.Parasites & vectors · 2023Article
- Infinity war:Microbial cell (Graz, Austria) · 2023Review
- The microRNA Cargo of Human Vaginal Extracellular Vesicles Differentiates Parasitic and Pathobiont Infections from Colonization by Homeostatic Bacteria.Microorganisms · 2023Article
- Distinct features of the host-parasite interactions between nonadherent and adherent Trichomonas vaginalis isolates.PLoS neglected tropical diseases · 2023Article
- The L-Rhamnose Biosynthetic Pathway inInternational journal of molecular sciences · 2022Article
- Seminal Plasma Glycoproteins as Potential Ligands of Lectins Engaged in Immunity Regulation.International journal of environmental research and public health · 2022Review
- Galectins as potential therapeutic targets in STIs in the female genital tract.Nature reviews. Urology · 2022Review
- Galectins - Important players of the immune response to CNS parasitic infection.Brain, behavior, & immunity - health · 2021Review
- Article
- Protozoan-Viral-Bacterial Co-Infections Alter Galectin Levels and Associated Immunity Mediators in the Female Genital Tract.Frontiers in cellular and infection microbiology · 2021Article
- Recent advances in the molecular biology of the protist parasiteFaculty reviews · 2021Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
Trichomoniasis is the most common non-viral sexually transmitted infection caused by the vaginotropic extracellular protozoan parasite Trichomonas vaginalis. The infection is recurrent, with no lasting immunity, often asymptomatic, and linked to pregnancy complications and risk of viral infection. The molecular mechanisms of immune evasion by the parasite are poorly understood. We demonstrate that galectin-1 and -3 are expressed by the human cervical and vaginal epithelial cells and act as pathogen-recognition receptors for the ceramide phosphoinositol glycan core (CPI-GC) of the dominant surface protozoan lipophosphoglycan (LPG). We used an in vitro model with siRNA galectin knockdown epithelial clones, recombinant galectins, clinical Trichomonas isolates, and mutant protozoan derivatives to dissect the function of galectin-1 and -3 in the context of Trichomonas infection. Galectin-1 suppressed chemokines that facilitate recruitment of phagocytes, which can eliminate extracellular protozoa (IL-8) or bridge innate to adaptive immunity (MIP-3α and RANTES (regulated on activation normal T cell expressed and secreted)). Silencing galectin-1 increased and adding exogenous galectin-1 suppressed chemokine responses to Trichomonas or CPI-GC/LPG. In contrast, silencing galectin-3 reduced IL-8 response to LPG. Live Trichomonas depleted the extracellular levels of galectin-3. Clinical isolates and mutant Trichomonas CPI-GC that had reduced affinity to galectin-3 but maintained affinity to galectin-1 suppressed chemokine expression. Thus via CPI-GC binding, Trichomonas is capable of regulating galectin bioavailability and function to the benefit of its parasitic survival. These findings suggest novel approaches to control trichomoniasis and warrant further studies of galectin-binding diversity among clinical isolates as a possible source for symptom disparity in parasitic infections.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.