Plasmodium falciparumInduces a Th1/Th2 Disequilibrium, Favoring the Th1‐Type Pathway, in the Human Placenta
Open Access
- 15 May 2001
- journal article
- research article
- Published by Oxford University Press (OUP) in The Journal of Infectious Diseases
- Vol. 183 (10) , 1530-1534
- https://doi.org/10.1086/320201
Abstract
During pregnancy, a local and systemic Th2 bias of maternal immunity favors Th1-dependent infections such as malaria. This study measured cytokines secreted in cultures of chorionic villi, placental blood cells (PBC), and serum in term placentas from 88 malaria-infected and -noninfected Cameroon women. Interleukin (IL)–2 and –4 were consistently low; IL-1β, IL-6, granulocyte-macrophage colony-stimulating factor, and transforming growth factor (TGF)–β2 were highest in villi cultures. Tumor necrosis factor (TNF)–α, interferon (IFN)–γ, and IL-10 were highest in PBC cultures. Malaria placental infection increased Th1-type cytokines, whereas Th2-type cytokines and TGF-β2 were unchanged. Addition of lipopolysaccharide or infected erythrocytes to cultures increased TNF-α, IL-1β, IL-6, and IL-10 secretions but not those of IFN-γ and IL-4. Overall, Plasmodium falciparum induced a placental immune response involving both Th1- and Th2-type cell activation. Although the Th1 pathway was favored, IL-10 secretion was also increased, and this increase should be effective in protecting the placenta by controlling the negative effects of Th1 cytokines on pregnancyKeywords
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