Abstract
BackgroundDuring pregnancy, syncytiotrophoblast vesicles contribute to maternal tolerance towards the fetus, but also to pathologies such as pre-eclampsia. The aim of the study was to address whether Plasmodium falciparum and HIV infections in pregnancy affect the secretion, microRNA content and function of trophoblast microparticles.MethodsMicroparticles were isolated and characterized from 122 peripheral plasmas of Mozambican pregnant women, malaria- and/or HIV-infected and non-infected. Expression of placenta-related microRNAs in microparticles was analysed by qPCR and the effect of circulating microparticles on dendritic cells assessed by phenotype analysis and cytokine/chemokine measurement.ResultsConcentrations of total and trophoblast microparticles detected by flow cytometry were higher in HIV-positive (P = 0.005 and P = 0.030, respectively) compared to non-infected mothers, as well as in women delivering low birthweight newborns (P = 0.032 and P = 0.021, respectively). miR-517c was overexpressed in mothers with placental malaria (P = 0.034), compared to non-infected. Microparticles from HIV-positive induced a higher expression of MHCII (P = 0.021) and lower production of MCP1 (P = 0.008) than microparticles from non-infected women.ConclusionsIn summary, alterations in total and trophoblast microparticles associated with malaria and HIV in pregnant women may have an immunopathogenic role. The potential for placental-derived vesicles and microRNAs as biomarkers of adverse outcomes during pregnancy and malaria infection should be confirmed in future studies.
Highlights
Infectious pathogens can alter the release and function of extracellular vesicles (EVs) to promote growth and induce transmission, evade host immune system and manipulate cellular microenvironment [1,2]
Concentrations of total and trophoblast microparticles detected by flow cytometry were higher in human immunodeficiency virus (HIV)-positive (P = 0.005 and P = 0.030, respectively) compared to non-infected mothers, as well as in women delivering low birthweight newborns (P = 0.032 and P = 0.021, respectively). miR-517c was overexpressed in mothers with placental malaria (P = 0.034), compared to non-infected
Microparticles from HIV-positive induced a higher expression of major histocompatibility complex II (MHCII) (P = 0.021) and lower production of Monocyte Chemoattractant Protein-1 (MCP1) (P = 0.008) than microparticles from non-infected women
Summary
Infectious pathogens can alter the release and function of extracellular vesicles (EVs) to promote growth and induce transmission, evade host immune system and manipulate cellular microenvironment [1,2]. Key players in functions mediated by EVs are secreted microRNAs (miRNAs), small non-coding RNAs that trigger either mRNA degradation or translational repression [5]. These EVs and miRNAs can be measured in body fluids and present a potential as diagnostic biomarkers [6,7], standardized procedures are lacking [8]. Exosome-like vesicles seem to be implicated in cell-to-cell communication between Plasmodium-infected red blood cells for the initiation of parasite sexual differentiation [14], and exosomes from Plasmodium yoelii-infected reticulocytes elicit protective immune responses against lethal infection in mice [15].
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