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01.12.2012 | Research | Ausgabe 1/2012 Open Access

Malaria Journal 1/2012

Mutations of complement lectin pathway genes MBL2 and MASP2 associated with placental malaria

Zeitschrift:
Malaria Journal > Ausgabe 1/2012
Autoren:
Ville Holmberg, Päivi Onkamo, Elisa Lahtela, Päivi Lahermo, George Bedu-Addo, Frank P Mockenhaupt, Seppo Meri
Wichtige Hinweise

Electronic supplementary material

The online version of this article (doi:10.​1186/​1475-2875-11-61) contains supplementary material, which is available to authorized users.

Competing interests

The authors declare that they have no competing interests.

Authors' contributions

VH designed the study, participated in the statistical analyses and drafted the manuscript. PO carried out the statistical analyses. EL participated in the genotyping. GBA participated in the recruitment of study participants and sample collection in Ghana. FPM coordinated the sample collection and participated in drafting the manuscript. SM participated in the study design and drafting the manuscript. All authors read and approved the final manuscript.

Abstract

Background

Innate immunity plays a crucial role in the host defense against malaria including Plasmodium falciparum malaria in pregnancy, but the roles of the various underlying genes and mechanisms predisposing to the disease are poorly understood.

Methods

98 single-nucletoide polymorphisms were genotyped in a set of 17 functionally related genes of the complement system in 145 primiparous Ghanaian women with placental malaria, defined by placental parasitaemia or malaria pigment, and as a control, in 124 non-affected primiparae.

Results

Placental malaria was significantly associated with SNPs in the lectin pathway genes MBL2, MASP2, FCN2 and in properdin. In particular, the main African mannose-binding lectin deficiency variant (MBL2* G57E, rs1800451) increased the odds of placental malaria (OR 1.6; permuted p-value 0.014). In contrast, a common MASP2 mutation (R439H, rs12085877), which reduces the activity of MBL-MASP2 complexes occurred in 33% of non-affected women and in 22% primiparae with placental malaria (OR 0.55, permuted p-value 0.020).

Conclusions

Excessive complement activation is of importance in the pathogenesis of placental malaria by mediating inflammation, coagulation, and endothelial dysfunction. Mutated MBL and MASP2 proteins could have direct intrinsic effects on the susceptibility to placental malaria, in addition to their roles in regulation of downstream complement activation.
Zusatzmaterial
Authors’ original file for figure 1
12936_2011_2035_MOESM1_ESM.tiff
Literatur
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