Plasmodium falciparum induces a Th1/Th2 disequilibrium, favoring the Th1-type pathway, in the human placenta

During pregnancy, a local and systemic Th2 bias of maternal immunity favors Th1-dependent infections such as malaria. This study measured cytokines se creted in cultures of chorionic villi, placental blood cells (PBC), and ser um in term placentas from 88 malaria-infected and -noninfected Cameroon wom en. Interleukin (IL)-2 and -4 were consistently low; IL-1 beta, IL-6, granu locyte-macrophage colony-stimulating factor, and transforming growth factor (TGF)-beta2 were highest in villi cultures. Tumor necrosis factor (TNF)-al pha, interferon (IFN)-gamma, and IL-10 were highest in PBC cultures. Malari a placental infection increased Th1-type cytokines, whereas Th2-type cytoki nes and TGF-beta2 were unchanged. Addition of lipopolysaccharide or infecte d erythrocytes to cultures increased TNF-alpha, IL-1 beta, IL-6, and IL-10 secretions but not those of IFN-gamma and IL-4. Overall, Plasmodium falcipa rum induced a placental immune response involving both Th1- and Th2-type ce ll activation. Although the Th1 pathway was favored, IL-10 secretion was al so increased, and this increase should be effective in protecting the place nta by controlling the negative effects of Th1 cytokines on pregnancy.