Abstract
Syncytiotrophoblast lines the intervillous space of the placenta and plays important roles in fetus growth throughout gestation. However, perturbations at the maternal-fetal interface during placental malaria may possibly alter the physiological functions of syncytiotrophoblast and therefore growth and development of the embryo in utero. An understanding of the influence of placental malaria on syncytiotrophoblast function is paramount in developing novel interventions for the control of placental pathology associated with placental malaria. In this review, we discuss how malaria changes syncytiotrophoblast function as evidenced from human, animal, and in vitro studies and, further, how dysregulation of syncytiotrophoblast function may impact fetal growth in utero. We also formulate a hypothesis, stemming from epidemiological observations, that nutrition may override pathogenesis of placental malaria-associated-fetal growth restriction. We therefore recommend studies on nutrition-based-interventional approaches for high placental malaria-risk women in endemic areas. More investigations on the role of nutrition on placental malaria pathogenesis are needed.
Highlights
Plasmodium falciparum is known to cause the most severe form of malaria, a disease that claims the lives of about one million people annually [1]
Malaria is associated with an increased risk of poor pregnancy outcomes, including maternal anemia, preterm delivery (PTD), and fetal growth restriction (FGR) which is defined as inability of the fetus to reach genetically predetermined size and weight at term [2]
We develop a model that describes the relationship between placental malaria FGR and the dysregulated syncytiotrophoblast function
Summary
Plasmodium falciparum is known to cause the most severe form of malaria, a disease that claims the lives of about one million people annually [1]. PTD, and FGR are major causes of malaria-associated low birth weight (LBW) babies. The overall prevalence of malaria-associated LBW babies from studies in endemic areas from year 1985 to 2000 has been estimated to be 20% of live births (reviewed in [3]). Placental malaria changes the environment in the intervillous space of placenta (Figure 1) It occurs as a result of P. falciparum infected erythrocytes (IE) binding to syncytiotrophoblast (ST), a continuous, multinucleated, specialized epithelia layer that covers interior of the villous of the placenta. While chronic placental malaria has been associated with an increased risk of FGR, acute placental malaria has been associated with PTD in malaria endemic areas [24]. We suggest a potential interventional approach targeting ST using evidence from epidemiological studies
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