IL-10 administration reduces the severity of the CNS inflammatory reaction associated with treatment of murine Trypanosoma brucei brucei infection

Abstract

Background Human African trypanosomiasis (HAT) is caused by Trypanosoma brucei rhodesiense or T.b. gambiense. Infection with either parasite is fatal if untreated. The disease has 2 clinical stages, the early-stage where the parasites proliferate in the blood and lymph and the CNS-stage where the parasites establish within the CNS. The only effective drug for treatment of both forms of CNS-stage trypanosomiasis is melarsoprol. Its use can cause the development of a post-treatment reactive encephalopathy (PTRE) characterised by a severe meningoencephalitis with infiltration of lymphocytes, macrophages and plasma cells. Astrocyte and microglial activation are also apparent. Various hypotheses exist regarding the pathogenesis of the PTRE. Recent evidence indicates that the balance of cytokines within the CNS may play a role in regulating the development of the PTRE and that IL-10 helps to protect the CNS from inflammatory pathology following early CNS invasion. This study investigates the therapeutic potential of IL-10 in a murine model of CNS-stage HAT.