ArticleJournal of innate immunity2019
Trichomonas vaginalis Induces NLRP3 Inflammasome Activation and Pyroptotic Cell Death in Human Macrophages.
Article in Journal of innate immunity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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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.
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Who cites it
20 citing papers in PubMed, 35 citations in OpenAlex.
- Differential Host Gene Expression Associated with Non-Research square · 2026Article
- Recent Advances in Biology, Host and Microbe Interactions of the Human Sexually Transmitted ParasiteInternational journal of molecular sciences · 2025Review
- Interactions between bacterial vaginosis-associated microbiota and Trichomonas vaginalis modulate parasite-induced pathogenicity and host immune responses.Parasites & vectors · 2025Article
- Trichomonas vaginalis extracellular vesicles activate the NLRP3 inflammasome and TLR3-mediated inflammatory cascades in host cells.PLoS pathogens · 2025Article
- NLRP3 Inflammasome in Gynecologic Inflammatory Diseases: Mechanisms, Pathophysiology, and Therapeutic Strategies.Journal of inflammation research · 2025Review
- Non-apoptotic regulated cell death mediates reprogramming of the tumour immune microenvironment by macrophages.Journal of cellular and molecular medicine · 2024Review
- Trichomonas vaginalis adherence phenotypes and extracellular vesicles impact parasite survival in a novel in vivo model of pathogenesis.PLoS neglected tropical diseases · 2023Article
- Effect of tumor-associated macrophages on the pyroptosis of breast cancer tumor cells.Cell communication and signaling : CCS · 2023Review
- Regulatory Functions of Hypoxia in Host-Parasite Interactions: A Focus on Enteric, Tissue, and Blood Protozoa.Microorganisms · 2023Review
- Infinity war:Microbial cell (Graz, Austria) · 2023Review
- The NLRP3 inflammasome recognizes alpha-2 and alpha-7.3 giardins and decreases the pathogenicity of Giardia duodenalis in mice.Parasites & vectors · 2023Article
- Establishment and application of a CRISPR-Cas12a-based RPA-LFS and fluorescence for the detection of Trichomonas vaginalis.Parasites & vectors · 2022Article
- Dec2 inhibits macrophage pyroptosis to promote periodontal homeostasis.Journal of periodontal & implant science · 2022Article
- Nod-like Receptors: Critical Intracellular Sensors for Host Protection and Cell Death in Microbial and Parasitic Infections.International journal of molecular sciences · 2021Review
- Recent advances in the molecular biology of the protist parasiteFaculty reviews · 2021Review
- NLRP3 Overexpression Associated With Poor Prognosis and Presented as an Effective Therapeutic Target in Osteosarcoma.Frontiers in pharmacology · 2021Article
- Neutrophil interactions with the sexually transmitted parasiteOpen biology · 2020Review
- Production and Functional Characterization of a Recombinant Predicted Pore-Forming Protein (TVSAPLIP12) ofFrontiers in cellular and infection microbiology · 2020Article
- NLRP3 Inflammasome From Bench to Bedside: New Perspectives for Triple Negative Breast Cancer.Frontiers in oncology · 2020Review
- Catch Me if You Can or Actors on the Run.Journal of innate immunity · 2019Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Trichomonas vaginalis is a sexually transmitted, eukaryotic parasite that causes trichomoniasis, the most common nonviral, sexually transmitted disease in the USA and worldwide. Little is known about the molecular mechanisms involved in the host immune response to this widespread parasite. Here we report that T. vaginalis induces NLRP3 inflammasome activation in human macrophages, leading to caspase-1 activation and the processing of pro-IL-1β to the mature and bioactive form of the cytokine. Using inhibitor-based approaches, we show that NLRP3 activation by T. vaginalis involves host cell detection of extracellular ATP via P2X7 receptors and potassium efflux. In addition, our data reveal that T. vaginalis inflammasome activation induces macrophage inflammatory cell death by pyroptosis, known to occur via caspase-1 cleavage of the gasdermin D protein, which assembles to form pores in the host cell membrane. We found that T. vaginalis-induced cytolysis of macrophages is attenuated in gasdermin D knockout cells. Lastly, in a murine challenge model, we detected IL-1β production in vaginal fluids in response to T. vaginalis infection in vivo. Together, our findings mechanistically dissect how T. vaginalis contributes to the production of the proinflammatory IL-1β cytokine and uncover pyroptosis as a mechanism by which the parasite can trigger host macrophage cell death.
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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.