title: Unlike the synchronous Plasmodium falciparum and P. chabaudi infection, the P. berghei and P. yoelii asynchronous infections are not affected by melatonin.
abstract: We have previously reported that Plasmodium chabaudi and P. falciparum sense the hormone melatonin and this could be responsible for the synchrony of malaria infection. In P. chabaudi and P. falciparum, melatonin induces calcium release from internal stores, and this response is abolished by U73122, a phospholipase C inhibitor, and luzindole, a melatonin-receptor competitive antagonist. Here we show that, in vitro, melatonin is not able to modulate cell cycle, nor to elicit an elevation in intracellular calcium concentration of the intraerythrocytic forms of P. berghei or P. yoelii, two rodent parasites that show an asynchrononous development in vivo. Interestingly, melatonin and its receptor do not seem to play a role during hepatic infection by P. berghei sporozoites either. These data strengthen the hypothesis that host-derived melatonin does not synchronize malaria infection caused by P. berghei and P. yoelii. Moreover, these data explain why infections by these parasites are asynchronous, contrary to what is observed in P. falciparum and P. chabaudi infections.
authors.affiliation: Departamento de Fisiologia, Instituto de Biociências, Universidade de São Paulo, São Paulo, Brazil.
authors.forename: Piero
authors.initials: P
authors.lastname: Bagnaresi
authors.forename: Eduardo
authors.initials: E
authors.lastname: Alves
authors.forename: Henrique
authors.initials: H
authors.lastname: Borges da Silva
authors.forename: Sabrina
authors.initials: S
authors.lastname: Epiphanio
authors.forename: Maria M
authors.initials: MM
authors.lastname: Mota
authors.forename: Célia Rs
authors.initials: CR
authors.lastname: Garcia