ArticleMethods (San Diego, Calif.)2017
Delineating neuroinflammation, parasite CNS invasion, and blood-brain barrier dysfunction in an experimental murine model of human African trypanosomiasis.
Article in Methods (San Diego, Calif.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed.
- Tau is necessary for Pseudomonas aeruginosa-induced blood-brain barrier dysfunction.Communications biology · 2026Article
- Leveraging microphysiological systems to expedite understanding of host-parasite interactions.PLoS pathogens · 2025Review
- Ginkgo biloba attenuated detrimental inflammatory and oxidative events due to Trypanosoma brucei rhodesiense in mice treated with melarsoprol.PLoS neglected tropical diseases · 2024Article
- How colonization bottlenecks, tissue niches, and transmission strategies shape protozoan infections.Trends in parasitology · 2023Review
- The murine meninges acquire lymphoid tissue properties and harbour autoreactive B cells during chronic Trypanosoma brucei infection.PLoS biology · 2023Article
- Application of diffusion weighted multiple boli ASL to a murine model of human African trypanosomiasis.Scientific reports · 2023Article
- Coenzyme QJournal of parasitic diseases : official organ of the Indian Society for Parasitology · 2023Article
- Live imaging of microglia during sleeping sickness reveals early and heterogeneous inflammatory responses.Frontiers in immunology · 2023Article
- The pathogenicity of blood stream and central nervous system forms ofF1000Research · 2022Article
- Microarray profiling predicts early neurological and immune phenotypic traits in advance of CNS disease during disease progression in Trypanosoma. b. brucei infected CD1 mouse brains.PLoS neglected tropical diseases · 2021Article
- The Actigraphy Sleep Score: A New Biomarker for Diagnosis, Disease Staging, and Monitoring in Human African Trypanosomiasis.The American journal of tropical medicine and hygiene · 2020Article
- Brain Delivery of Single-Domain Antibodies: A Focus on VHH and VNAR.Pharmaceutics · 2020Review
- Blood signatures for second stage human African trypanosomiasis: a transcriptomic approach.BMC medical genomics · 2020Article
- Generation of neuroinflammation in human African trypanosomiasis.Neurology(R) neuroimmunology & neuroinflammation · 2019Review
- Update on human African trypanosomiasis (sleeping sickness).Journal of neurology · 2019Review
- Using detergent-enhanced LAMP for African trypanosome detection in human cerebrospinal fluid and implications for disease staging.PLoS neglected tropical diseases · 2019Article
- PersistentInfection and immunity · 2019Article
- Clinical and Neuropathogenetic Aspects of Human African Trypanosomiasis.Frontiers in immunology · 2019Review
- Article
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3 authors.
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Abstract
Although Trypanosoma brucei spp. was first detected by Aldo Castellani in CSF samples taken from sleeping sickness patients over a century ago there is still a great deal of debate surrounding the timing, route and effects of transmigration of the parasite from the blood to the CNS. In this investigation, we have applied contrast-enhance magnetic resonance imaging (MRI) to study the effects of trypanosome infection on the blood-brain barrier (BBB) in the well-established GVR35 mouse model of sleeping sickness. In addition, we have measured the trypanosome load present in the brain using quantitative Taqman PCR and assessed the severity of the neuroinflammatory reaction at specific time points over the course of the infection. Contrast enhanced-MRI detected a significant degree of BBB impairment in mice at 14days following trypanosome infection, which increased in a step-wise fashion as the disease progressed. Parasite DNA was present in the brain tissue on day 7 after infection. This increased significantly in quantity by day 14 post-infection and continued to rise as the infection advanced. A progressive increase in neuroinflammation was detected following trypanosome infection, reaching a significant level of severity on day 14 post-infection and rising further at later time-points. In this model stage-2 disease presents at 21days post-infection. The combination of the three methodologies indicates that changes in the CNS become apparent prior to the onset of established stage-2 disease. This could in part account for the difficulties associated with defining specific criteria to distinguish stage-1 and stage-2 infections and highlights the need for improved staging diagnostics.
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