RESUMO
Both iron-deficient anemia (IDA) and malaria remain a threat to children in developing countries. Children with IDA are resistant to malaria, but the reasons for this are unknown. In this study, we addressed the mechanisms underlying the protection against malaria observed in IDA individuals using a rodent malaria parasite, Plasmodium yoelii (Py). We showed that the intra-erythrocytic proliferation and amplification of Py parasites were not suppressed in IDA erythrocytes and immune responses specific for Py parasites were not enhanced in IDA mice. We also found that parasitized IDA cells were more susceptible to engulfment by phagocytes in vitro than control cells, resulting in rapid clearance of parasitized cells and that protection of IDA mice from malaria was abrogated by inhibiting phagocytosis. One possible reason for this rapid clearance might be increased exposure of phosphatidylserine at the outer leaflet of parasitized IDA erythrocytes. The results of this study suggest that parasitized IDA erythrocytes are eliminated by phagocytic cells, which sense alterations in the membrane structure of parasitized IDA erythrocytes.
Assuntos
Anemia Ferropriva/imunologia , Eritrócitos/imunologia , Malária/imunologia , Fagocitose/imunologia , Plasmodium yoelii/imunologia , Imunidade Adaptativa , Animais , Linfócitos T CD4-Positivos/imunologia , Cálcio/metabolismo , Ensaio de Imunoadsorção Enzimática , Eritrócitos/química , Eritrócitos/parasitologia , Citometria de Fluxo , Imunidade Inata , Subunidade alfa de Receptor de Interleucina-2/imunologia , Malária/parasitologia , Malária/prevenção & controle , Membranas/química , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Nus , Fagócitos/imunologia , Fosfatidilserinas/imunologia , Plasmodium yoelii/crescimento & desenvolvimento , Plasmodium yoelii/patogenicidadeRESUMO
Cerebral malaria (CM) is the most severe complication of Plasmodium infection. Although inappropriate immune responses to Plasmodium falciparum are reported as the major causes of CM, the precise mechanisms for development remain unclear. IL-23 and IL-17 have critical roles in the onset of autoimmunity and inflammatory diseases triggered by microbial infections. Thus, we investigated the influence of IL-23 and IL-17 on experimental CM (ECM) using Plasmodium berghei ANKA infection of C57BL/6 mice. Both IL-23 deficient mice and wild-type (WT) mice developed ECM. IL-17 deficient mice also developed ECM, while IL-17 producing cells other than CD4(+) T cells (Th17) were increased in WT mice that developed ECM. In conclusion, this study showed that IL-23 and IL-17 are not involved in ECM development.