Unlike the synchronous Plasmodium falciparum and P. chabaudi infection, the P. berghei and P. yoelii asynchronous infections are not affected by melatonin

Original Research

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Authors: Piero Bagnaresi, Eduardo Alves, Henrique Borges da Silva, Sabrina Epiphanio, Maria M Mota, Célia RS Garcia

Published Date April 2009 Volume 2009:2 Pages 47 - 55

DOI: http://dx.doi.org/10.2147/IJGM.S3699

Piero Bagnaresi¹, Eduardo Alves¹, Henrique Borges da Silva¹, Sabrina Epiphanio², Maria M Mota², Célia RS Garcia¹

¹Departamento de Fisiologia, Instituto de Biociências, Universidade de São Paulo, São Paulo, Brazil; ²Unidade de Malária, Instituto de Medicina Molecular, Universidade de Lisboa, Lisboa, Portugal

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 melatoninreceptor 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 hostderived 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.

Keywords: malaria, calcium, melatonin, cell cycle, rhythm, sporozoite

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