title: Role of cytokines in Trypanosoma brucei-induced anaemia: A review of the literature.
abstract: BACKGROUND
  Anaemia is an important complication of trypanosomiasis. The mechanisms through which trypanosomal infection leads to anaemia are poorly defined. A number of studies have implicated inflammatory cytokines, but these data are limited and inconsistent. In this article, we reviewed the published literature on cytokines associated with Trypanosoma brucei infections and their role in the immunopathology leading to anaemia.
  
  
  METHODS
  Articles were searched in PubMed through screening of titles and abstracts with no limitation on date of publishing and study design. Articles in English were searched using keywords "African trypanosomiasis", "sleeping sickness", "Trypanosoma brucei", in all possible combinations with "anaemia" and/or "cytokines".
  
  
  RESULTS
  Twelve articles examining cytokines and their role in trypanosomeinduced anaemia were identified out of 1095 originally retrieved from PubMed. None of the articles identified were from human-based studies. A total of eight cytokines were implicated, with four cytokines (IFN-γ, IL-10, TNF-α, IL-12) showing an association with anaemia. These articles reported that mice lacking TNF-α were able to control anaemia, and that IFN-γ was linked to severe anaemia given its capacity to suppress erythropoiesis, while IL-10 was shown to regulate IFN-γ and TNF-α, providing a balance that was associated with severity of anaemia. IFN-γ and TNF-α have also been reported to work in concert with other factors such as nitric oxide and iron in order to induce anaemia.
  
  
  CONCLUSIONS
  IFN-γ, IL-10, and TNF-α were the three major cytokines identified to be heavily involved in anaemia caused by Trypanosoma brucei infection. The anti-inflammatory cytokine, IL-10, was shown to counter the effects of proinflammatory cytokines in order to balance the severity of anaemia. The mechanism of anaemia is multifactorial and therefore requires further, more elaborate research. Data from human subjects would also shed more light.
authors.affiliation: Department of Pathology, Microbiology Unit, College of Medicine, University of Malawi, Blantyre, Malawi.
authors.forename: J
authors.initials: J
authors.lastname: Musaya
authors.affiliation: Department of Biotechnical and Diagnostic Sciences, College of Veterinary Sciences, Animal Resource and Biosecurity, Makerere University, Kampala, Uganda.
authors.forename: E
authors.initials: E
authors.lastname: Matovu
authors.affiliation: Department of Medicine, College of Medicine, University of Malawi & Malawi-Liverpool Wellcome Trust Clinical Research Programme, Blantyre, Malawi.
authors.forename: M
authors.initials: M
authors.lastname: Nyirenda
authors.affiliation: Department of Basic Medical Sciences, Anatomy Unit, College of Medicine, University of Malawi, Blantyre, Malawi.
authors.forename: J
authors.initials: J
authors.lastname: Chisi
mesh_terms: D000740:Anemia / Q000097:blood / Q000276:immunology* / Q000469:parasitology; D000818:Animals; D016207:Cytokines / Q000096:biosynthesis / Q000276:immunology*; D007371:Interferon-gamma / Q000276:immunology; D016753:Interleukin-10 / Q000276:immunology; D051379:Mice; D014346:Trypanosoma brucei brucei / Q000276:immunology*; D014353:Trypanosomiasis, African / Q000150:complications / Q000276:immunology* / Q000469:parasitology; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology
chemical_list: D016207:Cytokines; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D007371:Interferon-gamma