Abstract
Background: Placental malaria is a major cause of infection induced adverse conditions in pregnancy and is attributed to the sequestration of malaria parasite in the intervillous space. We investigated if any relationship exists between the parasite density and cytokines in malaria parasite infected human placentas. Methods: Sixty (60) malaria parasite infected placentas from apparently healthy immediate post-partum women and 40 malaria parasite uninfected placentas which served as control were studied. Blood from the human placenta was aseptically collected and tested for HIV and malaria parasite using standard methods. Interferon-Gamma (IFNγ), Tumor Necrosis Factor alpha (TNFα), Interleukin-4 (IL-4), Interleukin-6 (IL-6) and Interleukin-10 (IL-10) were measured by Enzyme-Linked Immunosorbent Assay (ELISA) technique. Data were analysed using appropriate statistical tools. Results: The result revealed P. falciparum with a mean parasite density of 762.47±459.62 parasite/μl of blood. The mean±SD (11.71±6.55pg/ml) and 55.57±43.13pg/ml for IFNγ and IL-10 respectively for infected placenta was statistically higher on comparison with 5.58±2.86pg/ml and 16.60±4.88pg/ml for IFNγ and IL10 respectively for uninfected human placenta (P<0.05). Positive correlation existed between parasite density and IL-6 (r = 0.59, p = 0.001) and between parasite density and IL-10 (r =0.41, p=0.024). Conclusion: The study showed upregulated levels of IL-6 and IL-10 which indicates disruption of normal immune balance in the parasite infected placenta and the amount of IL-6 and IL-10 secreted could reflect the level of parasitaemia and could serve for diagnostic assessment of placental malaria.
Highlights
Malaria parasite adheres and sequesters in the endothelium of most organs in the trophoblastic villus epithelium of the placenta (Ayres Pereira et al, 2016)
As for P. falciparum, the infected erythrocytes accumulate in the intervillous space and binds to Chondroitin Sulfate-A (CSA) in the syncytiotrophoblast (Rieger et al, 2015; Pehrson et al, 2016)
The CSA is a glycosaminogen identified as host placental endothelial molecule associated with binding to VSA1, and this phenomenon favours the development of the parasite
Summary
Malaria parasite adheres and sequesters in the endothelium of most organs in the trophoblastic villus epithelium of the placenta (Ayres Pereira et al, 2016). Binding of the parasite, to the placental endothelium most times is accompanied by infiltration of mononuclear phagocytes in the intervillous space (Seitz et al, 2019) of which most of the leucocytes contain hemozoin; the malaria parasite pigments (Sharma & Shukla, 2017). The changes include the consumption and reduction in the amount of oxygen, glucose and other nutrients required for fetal development, the deposition of fibrinoid materials which culminates in thickening and lesion of the cytotrophoblastic membrane and disruption of normal immune balance due to increased secretion of cytokines (Sharma & Shukla, 2017). In response to invading pathogens such as malaria infection, the Type-2 dominance is reversed to Type-1 and this development may result in adverse pregnancy conditions (Lufele et al, 2017). Findings are expected to proffer solution to ensure successful delivery of healthy infants
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