ArticleVeterinary research communications2024
Bovine neutrophils kill the sexually-transmitted parasite Tritrichomonas foetus using trogocytosis.
Article in Veterinary research communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
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Who cites it
4 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Systematic Review of Vaccine Strategies Against Tritrichomonas foetus Infection in Cattle: Insights, Challenges, and Prospects.Parasite immunology · 2025Pooled it
- A Comprehensive Review of the Bovine Immune Response to Pathogens.International journal of molecular sciences · 2025Review
- Bovine trichomoniasis: A hidden threat to reproductive efficiency.Open veterinary journal · 2024Review
- The Biological Significance of Trogocytosis.Results and problems in cell differentiation · 2024Article
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Authors and funding
7 authors.
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Abstract
The protozoan parasite Tritrichomonas foetus (T. foetus) is the causative organism of bovine trichomonosis (also referred to as trichomoniasis), a sexually-transmitted infection that reduces fertility in cattle. Efforts to control trichomonosis on cattle farms are hindered by the discouragement of antibiotic use in agriculture, and the incomplete, short-lived protection conferred by the current vaccines. A more complete mechanistic understanding of what effective immunity to T. foetus entails could enable the development of more robust infection control strategies. While neutrophils, the primary responders to infection, are present in infected tissues and have been shown to kill the parasite in vitro, the mechanism they use for parasite killing has not been established. Here, we show that primary bovine neutrophils isolated from peripheral blood rapidly kill T. foetus in vitro in a dose-dependent manner, and that optimal parasite killing is reduced by inhibitors of trogocytosis. We also use imaging to show that bovine neutrophils surround T. foetus and trogocytose its membrane. These findings are consistent with killing via trogocytosis, a recently described novel neutrophil antimicrobial mechanism.
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