In Africa, most of the malaria mortality and morbidity is borne by children and pregnant women with an estimate 200,000 infant deaths each year as a result of malaria infection in pregnancy . During placental malaria (PM) parasites accumulate in the placenta with an increased risk of low birth weight (LBW) . This accumulation can be related to low blood flow through the placenta and to specific adhesion of infected red blood cells (IRBCs) on syncytiotrophoblast. This adhesion is mediated by chondroitin sulphate A and specific var antigens. Monocytes also accumulate in the intervillous space of the placenta  mostly attracted by release of MIF [4, 5]. Pro-inflammatory cytokine release also associates with this accumulation of parasites, pigment, and monocytes in the tissue [6, 7].
Decreased blood flow in the placenta is the major factor triggering LBW, which had previously been linked to a modulation of placental cytokine expression . In this context, prostaglandins (PGs) are important modulators of vascular perfusion and fever . Conversion of arachidonic acid to PGs is catalyzed by two isoforms of cyclooxygenase (COX-1 and COX-2) . COX-2-generated PGs are important in inflammation and host defence and is up-regulated prior to the onset of labour [10, 11]. Whereas COX-1-generated PGs is implicated in homeostasis and survival of the foetus, and mainly secreted in decidual lining of the uterus [12, 13] without modulation during gestation or labour. The role of COX-1 and -2 during placental pathology was suspected some time ago when bacterial lipopolysaccharide mediated foetal death was related to an over-production of COX-2 . In the same line COX-2 over expression was reported during pre-eclampsia , but not after this episode  and was associated with apoptosis in smooth chorion trophoblast cells of human foetal membrane tissues . This enhancement seems to be triggered by leukocyte microparticles [15, 18]. However, Khan et al published conflicting results describing a reduction of COX-2 and of the amount of NHE-1 in pre-eclamptic placentas with an unaltered level of COX-1 .
During placental malaria, modulation of these PGs pathway could play a role in preterm delivery and low birth weight as observed during pre-eclampsia. A foetal COX-2 gene polymorphism was associated with placental malperfusion during placental malaria . In the general, circulation PGE2 and blood mononuclear cell COX-2 expression were also reported to be inversely related with disease severity in children with malaria [21, 22].
Two other arachidonic acid pathways, the epoxide and the lipoxygenase (LOX) pathway , are involved in pathology during pregnancy . LOX leads to synthesis of leukotrienes and lipoxins with immune and anti-inflammatory activity. Three enzymes control this pathway: 5-LOX produced by neutrophils, 12-LOX produced by platelets, and 15-LOX located in macrophages and endothelia. 15-LOX is highly inducible and produces hydroxyeicosatetraenoic (HETE) compounds . Interestingly, 15-HETE is a powerful inhibitor of pro-inflammatory eicosanoids, whereas 5-HETE and 12-HETE are chemotactic factors for neutrophils and they also stimulate vasodilation through PG synthesis .
Eicosanoids are thus powerful regulators of placenta perfusion and overall of the pregnancy outcome. New analgesic and anti-inflammatory drugs, inhibitors of COX activity, are often used in malaria endemic areas to reduce fever, pain, and inflammation . They can interfere with PGs regulations and modulate the outcome of the pregnancy even if antenatal administration of celecoxib (a COX-2 inhibitor) seems to improve placental perfusion in the pregnant rabbit . All these data pave the way of new studies to understand the pathophysiology of placental malaria, and this study was designed to address the role of these enzymes during PM in low malaria transmission area. The purpose of this study was to evaluate the levels of COX-1, COX-2, and 15-LOX mRNA genes in human placenta infected by P. falciparum compared to uninfected placenta. Although delivery is only an instant in the whole pregnancy, it is however a good snapshot of the placenta statement. Studies conducted at delivery also give information on the late stage of the mother-baby interaction.