Iron Homeostasis and Trypanosoma brucei Associated Immunopathogenicity Development: A Battle/Quest for Iron

Figure 1

Lifecycle of African trypanosomes. Tsetse flies become infected following a blood meal taken from a trypanosome infected mammalian host. The parasites that are taken up reach the midgut together with the blood meal. Subsequently, only the short stumpy (non-dividing) forms of the parasite that are preadapted to the changed environment within the tsetse fly will be able to differentiate into procyclic forms. The multiplying procyclic forms colonize the ectoperitrophic space, after which they migrate to the salivary glands via the proventriculus lumen to move into the foregut and proboscis. During this migration, the procyclic forms in the fly differentiate into epimastigote forms that within the salivary glands attach to the epithelium and proliferate, giving rise to metacyclic forms which are preadapted for survival into the mammalian host [16, 17]. Upon a blood meal on a new host, the parasites will be inoculated and differentiate into a long slender (dividing) form. Within the mammalian host long slender forms multiply via binary fission, giving rise to a first peak of parasitemia. When the trypanosome population reaches a sufficiently high density, a quorum sensing-like mechanism elicits the differentiation of long slender forms into short stumpy forms that allow transmission following uptake by a new tsetse fly [18, 19]. During the entire lifecycle of trypanosomes, there is a continuous fight for iron acquisition at the level of both the parasites and the host. Image generated by Joar Pinto.