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Distinct placental malaria pathology caused by different Plasmodium berghei lines that fail to induce cerebral malaria in the C57BL/6 mouse

Lurdes Rodrigues-Duarte1, Luciana Vieira de Moraes1, Renato Barboza2, Claudio RF Marinho2, Blandine Franke-Fayard3, Chris J Janse3 and Carlos Penha-Gonçalves1*

Author Affiliations

1 Instituto Gulbenkian de Ciência, Rua da Quinta Grande, 06, Oeiras, 2780-156, Portugal

2 Department of Parasitology, Instituto de Ciências Biomédicas, University of São Paulo, São Paulo, Brazil

3 Leiden Malaria Research Group, Parasitology, Leiden University Medical Center, Leiden, The Netherlands

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Malaria Journal 2012, 11:231  doi:10.1186/1475-2875-11-231

Published: 16 July 2012



Placental malaria (PM) is one major feature of malaria during pregnancy. A murine model of experimental PM using BALB/c mice infected with Plasmodium berghei ANKA was recently established, but there is need for additional PM models with different parasite/host combinations that allow to interrogate the involvement of specific host genetic factors in the placental inflammatory response to Plasmodium infection.


A mid-term infection protocol was used to test PM induction by three P. berghei parasite lines, derived from the K173, NK65 and ANKA strains of P. berghei that fail to induce experimental cerebral malaria (ECM) in the susceptible C57BL/6 mice. Parasitaemia course, pregnancy outcome and placenta pathology induced by the three parasite lines were compared.


The three P. berghei lines were able to evoke severe PM pathology and poor pregnancy outcome features. The results indicate that parasite components required to induce PM are distinct from ECM. Nevertheless, infection with parasites of the ANKAΔpm4 line, which lack expression of plasmepsin 4, displayed milder disease phenotypes associated with a strong innate immune response as compared to infections with NK65 and K173 parasites.


Infection of pregnant C57BL/6 females with K173, NK65 and ANKAΔpm4 P. berghei parasites provide experimental systems to identify host molecular components involved in PM pathogenesis mechanisms.

Plasmodium berghei; Placental malaria; Cerebral malaria; Placental pathology; TNF; TLR4; TLR2