ORIGINAL RESEARCH article
Front. Parasitol.
Sec. Immunity and Immune Evasion
Roles of cytokines in modulating Trypanosoma brucei rhodesiense infection outcomes in vervet monkeys
Provisionally accepted
Clarah Jebet1John Kibuthu Thuita2,3
Daniel Masiga4Benedict Owino Orindi5John Oidho6
Mark C Field7Enock Matovu8
Vincent Owino Adung'a1,9*- 1Department of Biochemistry and Molecular Biology,, Njoro, Kenya
- 2Meru University of Science and Technology, Meru, Kenya
- 3Department of Animal Sciences, School of Agriculture and Food Sciences, Meru, Kenya
- 4Department of Molecular Biology, International Centre of Insect Physiology and Ecology (icipe), Nairobi, Kenya
- 5Department of Public Health and Public Care, Leuven Biostatistics and Statistical Bioinformatics Centre, Leuven, Belgium
- 6Biotechnology Research Institute - Kenya Agricultural and Livestock Research Organisation, Chemotherapy Division,, Kikuyu, Kenya
- 7Institute of Parasitology, Czech Academy of Sciences,, České Budějovice, Czechia
- 8Department of Biomedical Laboratory Technology and Molecular Biology, College of Veterinary Medicine, Animal Resources and Biosecurity (COVAB), Makerere University, Kampala, Uganda
- 9Egerton University, Njoro, Kenya
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Human African trypanosomiasis (HAT), caused by Trypanosoma brucei rhodesiense, is categorised as acute due to rapid disease progression, but presents varying clinical outcomes. Although the mechanisms underpinning differential clinical progression are poorly understood, both host and parasite factors are implicated. Here, we assessed the roles of selected host cytokines in disease progression using a tsetse-mediated infection in non-human primate (NHP) vervet monkey model that closely mimics HAT and natural infection. We quantified eight cytokines, including TNF-α, IFN-γ, IL-10, IL-6, IL-12 and IL-1 β, brain injury biomarker S100β, clinical data and compared acute and chronic infections. Monkeys infected with KETRI 3801 and KETRI 3928 had a mean survival time of 28 and 95 days respectively. In both infected groups, cytokine levels were significantly higher than uninfected controls (p<0.05). IL-12, IL-6 and IL-1β cytokines were significantly elevated (p<0.05) in early-stage to the onset of late-stage disease. IL-1β, IL-6, IL-12 and IL-10 are implicated in pro-and counter inflammatory responses. In addition, CSF parasite and WBC levels were higher in KETRI 3801 as compared to KETRI 3928 infections. We conclude that cytokines play roles in modulating disease progression and severity in a NHP model of HAT, and this is important in understanding varying infection outcomes.
Keywords: African trypanosomiasis, Cytokines, immune response, Immunomodulation, Infection, Trypanosoma brucei rhodesiense
Received: 15 Oct 2025; Accepted: 12 Dec 2025.
Copyright: © 2025 Jebet, Thuita, Masiga, Orindi, Oidho, Field, Matovu and Adung'a. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Vincent Owino Adung'a
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