Plasma cytokines quantification among Trypanosoma brucei rhodesiense sleeping sickness cases and controls in Rumphi, Malawi

Kelita Kamoto TrypanoGEN Research Group, members of The H3Africa Consortium Arthur Chiwaya TrypanoGEN Research Group, members of The H3Africa Consortium Peter Nambala TrypanoGEN Research Group, members of The H3Africa Consortium Pricilla Chammudzi TrypanoGEN Research Group, members of The H3Africa Consortium Edward Senga TrypanoGEN Research Group, members of The H3Africa Consortium John Chisi TrypanoGEN Research Group, members of The H3Africa Consortium Enock Matovu TrypanoGEN Research Group, members of The H3Africa Consortium Janelisa Musaya TrypanoGEN Research Group, members of The H3Africa Consortium

Keywords: Sleeping sickness, Human African Trypanosomiasis , Trypanosoma brucei rhodesiense , Plasma cytokines, IL-8, TNF-α, IL-10

Abstract

Introduction
Trypanosoma brucei (T.b.) rhodesiense is the cause of the acute form of human African trypanosomiasis (HAT) in eastern and southern  African countries, including Malawi. For a long time, untreated HAT infections were believed to be 100% fatal. However, recent studies  show that infection by T.b. rhodesiense can result in a wide range of clinical outcomes in its human host. Apart from other factors such  as parasite diversity, cytokines have been strongly implicated to play a major role in the outcome of T.b. rhodesiense infections. In this study, we quantify the levels of three cytokines Interleukin-8 (IL-8), Tumor Necrotic Factor alpha (TNF-α) and Interleukin -10 (IL-10) in plasma amongst HAT cases (treated and untreated) and controls recruited during medical survey.
Methods
Two-hundred and thirty-three plasma samples (HAT cases and controls) from Rumphi, one of the endemic areas in Malawi were used.  Blood collected was centrifuged, plasma extracted and stored in cryovials at -800 C until processing. Plasma cytokine concentration was measured using ELISA.
Results
Plasma samples for 233 individuals, 76 HAT cases and 157 controls were quantified. Among the cases, nine had their plasma collected before treatment (untreated) and the rest were treated before blood for plasma analysis was collected. Controls had significantly higher mean plasmatic levels of TNF-α (94.5 ±474.12 pg/ml) and IL-8 (2258.6 ±5227.4 pg/ml) than cases TNF-α (29.35±181.58 pg/ml) and IL-8 (1191.3±4236.09 pg/ml). Controls and cases had similar mean levels of IL-10 in plasma. Only IL-8 had statistically significant higher median levels in the untreated than treated HAT cases P=0.006.
Conclusion
Our data suggest that cytokines could be considered as biomarkers of HAT infection and treatment. Further studies with a larger cohort of cases and additional cytokines which are known to be associated with HAT infection outcomes will be required to evaluate these cytokines further.

Section

Original Research

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