FIGURE 3.

LD in the biological cycles of protozoan parasites. Trypanosoma cruzi displays reservosomes (R) in epimastigotes and cytoplasmic LD in metacyclic trypomastigotes (MT) that mainly store cholesterol and SE, respectively. While degradation of R occurs during metacyclogenesis, the contact with the host cell induces the production of LD and PGE2 in MT and in the host cell favoring T. cruzi infection and replication. Toxoplasma gondii expresses TgDGAT1, TgACAT1 and TgACAT2, which are the enzymes responsible for the LD synthesis in the parasite. An increased number of host LD was observed in cells containing vacuoles with tachyzoites, which is the characteristic parasite stage of the acute infection. These LD are also observed in the vacuole lumen and inside the parasite cytoplasm, thus evidencing the transport of host lipids to the parasite. Leishmania spp. increases the LD number during the evolution from procyclic to metacyclic promastigotes, which also contain PGF2α, suggesting a role of this eicosanoid as a parasite virulence factor. Host’s LD are also increased in macrophages infected with Leishmania. Like T. gondii, these host LD have been observed inside the Leishmania vacuole and even in the parasite’s cytoplasm. Plasmodium was found to store NL in the food vacuole. NL are important to prevent heme toxicity by production of the malaria pigment hemozoin. Infected red-blood cells increase the number and size of LD when they evolve from the trophozoite to squizont form, whereas LD breakdown characterizes merozoite maturation and release together with FA.