ArticleParasitology research2019
Trichomonas vaginalis triggers the release of THP-1 extracellular traps.
Article in Parasitology research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Immunomodulatory Effects of the Antimicrobial Peptide KR-20: Implications for Trichomoniasis.Molecules (Basel, Switzerland) · 2026Article
- Pentatrichomonas hominis induces extracellular traps formation of macrophages via the TLR2/NADPH/PAD4 pathway.Parasites & vectors · 2025Article
- Early responses of primary human and bovine monocytes, monocytic THP-1 cells and THP-1 cell-derived macrophages to vitalFrontiers in immunology · 2025Article
- Infinity war:Microbial cell (Graz, Austria) · 2023Review
- Proteomic analysis reveals changes in the proteome of human THP-1 macrophages infected withFrontiers in cellular and infection microbiology · 2023Article
- Bystander effect of SARS-CoV-2 spike protein on human monocytic THP-1 cell activation and initiation of prothrombogenic stimulus representing severe COVID-19.Journal of inflammation (London, England) · 2022Article
- Article
- Establishment and application of a CRISPR-Cas12a-based RPA-LFS and fluorescence for the detection of Trichomonas vaginalis.Parasites & vectors · 2022Article
- Trichomonas vaginalis triggers neutrophil extracellular traps reducing parasite integrity and growth.Parasitology research · 2022Article
- The State of Art of Extracellular Traps in Protozoan Infections (Review).Frontiers in immunology · 2021Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Trichomonas vaginalis is responsible for the prevalence of trichomoniasis, which may be one of the most epidemic nonviral sexually transmitted pathogens. Extracellular traps (ET) are a unique form of innate immunity against infection; they bind to and kill microorganisms. However, the effect of T. vaginalis on ET release in the human monocytic cell line THP-1 remains unclear. In the present study, the morphology of ET derived from THP-1 in response to T. vaginalis was observed by scanning electron microscopy (SEM). The results demonstrated ET entangling T. vaginalis. Then, the colocalization of histone (H3) and myeloperoxidase (MPO) with DNA was observed via fluorescence confocal microscopy. Colocalization revealed the classic characteristics of DNA decorated with H3 and MPO. T. vaginalis significantly increased reactive oxygen species (ROS) and THP-1-derived ET. In addition, we measured the levels of lactic dehydrogenase (LDH) and the phosphorylation of the P38 and ERK1/2 MAPK signaling pathways. The results indicated that the formation of ET induced by T. vaginalis was related to phosphorylation of the P38 and ERK1/2 MAPK signaling pathways but not to LDH levels. These data confirmed the phenomenon of THP-1-derived ET being triggered by T. vaginalis in vitro; this process may play a pivotal role in innate immunity during defense against T. vaginalis infection.
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