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

Piero Bagnaresi, Eduardo Alves, Henrique Borges Da Silva, Sabrina Epiphanio, Maria M. Mota, Célia Regina Da Silva Garcia

Research output: Contribution to journalArticlepeer-review

34 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)47-55
Number of pages9
JournalInternational Journal of General Medicine
Volume2
StatePublished - 2009
Externally publishedYes

Keywords

  • Calcium
  • Cell cycle
  • Malaria
  • Melatonin
  • Rhythm
  • Sporozoite

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