The understanding of host immune mechanisms during Plasmodium infection is essential to improve malaria prevention. In malaria endemic regions, one single person can be infected simultaneously with different species or strains of the same specie of Plasmodium, a phenomenon named superinfection. Semi-immune young children can be protected against superinfection. It was described in experimental rodent malaria that ongoing blood-stage infection can inhibit the development of secondary liver-stage infection. This protection is dependent on parasitemia and on the iron regulator hormone, hepcidin. Hepcidin levels increase in the liver during blood-stage Plasmodium chabaudi or Plasmodium berghei malaria. This augment leads to decrease of iron availability in hepatocytes, inhibiting the development of liver-stage forms of P. berghei. In addition, blood-stage infection causes intense liver inflammation and necrosis what, in turns, could protect against a subsequent infection with sporozoites. We have recently shown that IL-1alpha is produced at high levels in the liver during blood-stage P. chabaudi malaria and this cytokine is essential for inflammatory cell recruitment, pro-inflammatory cytokine production and development of hepatic necrosis. The aim of the present project is to evaluate the influence of IL-1alpha produced in the liver during blood-stage Plasmodium infection may have in a secondary liver-stage infection and its role in the protection against superinfection.
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