ABSTRACT
Background: During pregnancy, the balanced dominance of the T helper17 response shifts to a Th2 response that is characterised by the production of IL-10, following the completion of the implantation process. Transforming growth factor-β (TGF-β) expression is associated with the completion of trophoblast invasion and placental growth. This study assessed the effect of malaria infection on the levels of IL-17, IL-10, and TGF-β in the plasma of pregnant mice with malaria. Methods: Seventeen pregnant BALB/C mice were divided into two groups: mice infected with Plasmodium berghei (treatment group) and uninfected mice (control group). The mice were sacrificed on day 18 post-mating. Parasitemia was measured by Giemsa staining. The levels of IL-17, IL-10, and TGF-β were measured by ELISA. Results: Using independent t test, the IL-17 levels in the treatment group were higher than those in the control group (P = 0.040). The IL-10 levels in the treatment group were lower than those in the control group (P = 0.00). There was no significant difference in the TGF-β levels (P = 0.055) between two groups. However, using SEM analysis the degree of parasitemia decreased the plasma TGF-β levels (tcount = 5.148; ≥ ttable = 1.96). SEM analysis showed that a high degree of parasitemia increased the IL-17 levels and decreased the IL-10 and TGF-β levels. Conclusion: Malaria infection during pregnancy interferes with the systemic balance by increasing the IL-17 levels and decreasing the IL-10 and TGF-β levels.
ABSTRACT
The sequestration of infected erythrocytes in the placenta can activate the syncytiotrophoblast to release cytokines that affect the micro-environment and influence the delivery of nutrients and oxygen to fetus. The high level of IL-10 has been reported in the intervillous space and could prevent the pathological effects. There is still no data of Th17 involvement in the pathogenesis of placental malaria. This study was conducted to reveal the influence of placental IL-17 and IL-10 levels on fetal weights in malaria placenta. Seventeen pregnant BALB/C mice were divided into control (8 pregnant mice) and treatment group (9 pregnant mice infected by Plasmodium berghei). Placental specimens stained with hematoxylin and eosin were examined to determine the level of cytoadherence by counting the infected erythrocytes in the intervillous space of placenta. Levels of IL-17 and IL-10 in the placenta were measured using ELISA. All fetuses were weighed by analytical balance. Statistical analysis using Structural Equation Modeling showed that cytoadherence caused an increased level of placental IL-17 and a decreased level of placental IL-10. Cytoadherence also caused low fetal weight. The increased level of placental IL-17 caused low fetal weight, and interestingly low fetal weight was caused by a decrease of placental IL-10. It can be concluded that low fetal weight in placental malaria is directly caused by sequestration of the parasites and indirectly by the local imbalance of IL-17 and IL-10 levels.