Publicação
Cytoadherence capabilities of Plasmodium berghei ANKA and NK65 infected red blood cells in different malaria models
| Resumo: | Malaria is an infectious disease caused by an intracellular parasite (genus Plasmodium). Sequestration of mature erythrocytic forms of P. falciparum is a key factor in the development of severe malaria-associated pathologies, namely CM. Brains of patients that died of CM show a preferential sequestration of the MF, and blood-smears of malaria patients at hospital admission show exclusively immature erythrocytic forms. Recently, it was demonstrated that in PbA-infected C576BL/6 mice, an experimental cerebral malaria model, there is accumulation of pRBCs in the brain, as well as CD8+T cells. On the contrary, PbA-infected Balb/C mice, which don‟t develop ECM, don‟t accumulate these cell-populations. PbNK65-infected C57BL/6 mice also don‟t develop ECM, though they accumulate CD8+T cells in the brain, but not infected erythrocytes. Using these models of malaria, our main goal was to study the blood-stage dynamics and sequestration capabilities of both parasite strains and associate that pattern with the pathology. Results show that MF of both parasite strains are not seen in circulation at a certain point in infection. Also, this disappearance from circulation is concomitant with sequestration of PbA schizonts in the spleen and lungs (C57BL/6 mice), as well as in the fat tissue and liver (both hosts). In addition, we wanted to clarify the importance of parasite versus host in cytoadherence of pRBCs to the brain microvasculature. Our results suggest that the absence of PbNK65 sequestration in the brain of C57BL/6 mice is mainly due to differences between this parasite and PbA in its intrinsic cytoadherence capability. Moreover, we observed a significant difference in numbers of merozoites formed per schizont between PbNK65 and PbA infections, which might account for the differences in parasitaemia growth rates and infectivity that have been described for these strains. |
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| Autores principais: | Albuquerque, Maria Inês Sousa de, 1988 |
| Assunto: | Malária Plasmodium berghei Parasitas Anopheles Teses de mestrado - 2011 |
| Ano: | 2011 |
| País: | Portugal |
| Tipo de documento: | dissertação de mestrado |
| Tipo de acesso: | acesso aberto |
| Instituição associada: | Universidade de Lisboa |
| Idioma: | inglês |
| Origem: | Repositório da Universidade de Lisboa |
| Resumo: | Malaria is an infectious disease caused by an intracellular parasite (genus Plasmodium). Sequestration of mature erythrocytic forms of P. falciparum is a key factor in the development of severe malaria-associated pathologies, namely CM. Brains of patients that died of CM show a preferential sequestration of the MF, and blood-smears of malaria patients at hospital admission show exclusively immature erythrocytic forms. Recently, it was demonstrated that in PbA-infected C576BL/6 mice, an experimental cerebral malaria model, there is accumulation of pRBCs in the brain, as well as CD8+T cells. On the contrary, PbA-infected Balb/C mice, which don‟t develop ECM, don‟t accumulate these cell-populations. PbNK65-infected C57BL/6 mice also don‟t develop ECM, though they accumulate CD8+T cells in the brain, but not infected erythrocytes. Using these models of malaria, our main goal was to study the blood-stage dynamics and sequestration capabilities of both parasite strains and associate that pattern with the pathology. Results show that MF of both parasite strains are not seen in circulation at a certain point in infection. Also, this disappearance from circulation is concomitant with sequestration of PbA schizonts in the spleen and lungs (C57BL/6 mice), as well as in the fat tissue and liver (both hosts). In addition, we wanted to clarify the importance of parasite versus host in cytoadherence of pRBCs to the brain microvasculature. Our results suggest that the absence of PbNK65 sequestration in the brain of C57BL/6 mice is mainly due to differences between this parasite and PbA in its intrinsic cytoadherence capability. Moreover, we observed a significant difference in numbers of merozoites formed per schizont between PbNK65 and PbA infections, which might account for the differences in parasitaemia growth rates and infectivity that have been described for these strains. |
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