Syncytiotrophoblast Functions and Fetal Growth Restriction during Placental Malaria: Updates and Implication for Future Interventions

Figure 1

The microenvironment in the intervillous space of the placenta during active placental malaria: (a) Interaction of parasite ligand, VAR2CSA [10, 12] with CSA that is expressed by ST [8, 13]. (b) Recognition of parasite bioactive molecules of schizogony by surface PRRs expressed by both maternal macrophages and fetal syncytiotrophoblast; that is, malarial GPI-anchor bind TLR1/TLR2 or TLR2/TLR6 [14], and parasite’s DNA is recognized by TLR9 [15] and hemozoin by TLR9 (see [16] and inflammasome (NALP3) [17]). (c) Inflammation in the IVS is attributed to chemokines and cytokines secreted by maternal macrophages, monocytes, and T cell as well as ST [15, 16, 18–20]. (HA: hyaluronic acid; CSA: chondroitin sulphate A; IVS: intervillous space; NALP3: inflammasome; GPI: glycosylphosphatidylinositol; IE: infected erythrocyte; E: erythrocyte).