Abstract
Immunopathology of placental malaria is most significant in women in their first pregnancy especially in endemic areas, due to a lack of protective immunity to Plasmodium falciparum, which is acquired in successive pregnancies. In some studies (but not all), grand multigravidae (defined as 5 or more pregnancies, G5–7) are more susceptible to poor birth outcomes associated with malaria compared to earlier gravidities. By comparing peripheral cellular responses in primigravidae (G1), women in their second to fourth pregnancy (G2–4) and grand multigravidae we sought to identify key components of the dysregulated immune response. PBMC were exposed to CS2-infected erythrocytes (IE) opsonised with autologous plasma or unopsonised IE, and cytokine and chemokine secretion was measured. Higher levels of opsonising antibody were present in plasma derived from multigravid compared to primigravid women. Significant differences in the levels of cytokines and chemokines secreted in response to IE were observed. Less IL-10, IL-1β, IL-6 and TNF but more CXCL8, CCL8, IFNγ and CXCL10 were detected in G5–7 compared to G2–4 women. Our study provides fresh insight into the modulation of peripheral blood cell function and effects on the balance between host protection and immunopathology during placental malaria infection.
Highlights
Placental malaria due to Plasmodium falciparum infection is characterised by the accumulation of infected erythrocytes (IE) in the intervillous spaces of the placenta
Levels of opsonising antibody were assessed using a THP-1 phagocytosis assay in which CS2 IE were opsonised with heat inactivated (HI) plasma derived from primigravid and multigravid women who were further divided into secundigravidae to gravidae 4 (G2– 4) and grand multigravidae (G5–7)
This study explored the role of gravidity in modifying the early cellular immune response of pregnant women to P. falciparum IE
Summary
Placental malaria due to Plasmodium falciparum infection is characterised by the accumulation of infected erythrocytes (IE) in the intervillous spaces of the placenta. Immunopathology of pregnancy-specific malaria is largely confined to women in their first and second pregnancy due to a lack of protective immunity, and results in increased risk of severe anemia and low birth weight (LBW), especially in highly endemic areas [1]. These complications are associated with monocyte and macrophage accumulation in the maternal intervillous circulation of the placenta, termed intervillositis [2], and with increased placental blood TNF [3]. Waning immunity was mooted as an explanation, but no confirmatory studies were reported
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