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01.12.2012 | Research | Ausgabe 1/2012 Open Access

Malaria Journal 1/2012

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

Zeitschrift:
Malaria Journal > Ausgabe 1/2012
Autoren:
Lurdes Rodrigues-Duarte, Luciana Vieira de Moraes, Renato Barboza, Claudio RF Marinho, Blandine Franke-Fayard, Chris J Janse, Carlos Penha-Gonçalves
Wichtige Hinweise

Electronic supplementary material

The online version of this article (doi:10.​1186/​1475-2875-11-231) contains supplementary material, which is available to authorized users.
Lurdes Rodrigues-Duarte, Luciana Vieira de Moraes contributed equally to this work.

Competing interests

All authors have declared no conflict of interest.

Authors’ contributions

LRD and LVM conceived and designed the research/study, performed experiments, analysed data and wrote the paper; CPG conceived and designed the research/study, analysed data, wrote the paper; CRFM and RB performed morphometric analysis, analysed and discussed data; BFF and CJJ provided materials, reviewed and discussed the experimental data and wrote the paper. All authors read and approved the manuscript.

Abstract

Background

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.

Methods

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.

Results

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.

Conclusions

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.
Zusatzmaterial
Additional file 1: Table. Infection during pregnancy increases the percentage of stillbirths. (DOC 29 KB)
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Additional file 2: Figure. Gene expression of inflammatory factors in non-infected placentas. Placentas from healthy pregnant females were collected at G18 or G19 and RNA expression of Ccl2, Ccl3, Tlr2, Tlr4 and Tnfα genes were evaluated by qReal Time PCR. Relative quantification (RQ) was obtained with normalization by GAPDH. *p<0.05. (TIFF 3 MB)
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