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      Does Malaria Affect Placental Development? Evidence from In Vitro Models

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          Abstract

          Background

          Malaria in early pregnancy is difficult to study but has recently been associated with fetal growth restriction (FGR). The pathogenic mechanisms underlying malarial FGR are poorly characterized, but may include impaired placental development. We used in vitro methods that model migration and invasion of placental trophoblast into the uterine wall to investigate whether soluble factors released into maternal blood in malaria infection might impair placental development. Because trophoblast invasion is enhanced by a number of hormones and chemokines, and is inhibited by pro-inflammatory cytokines, many of which are dysregulated in malaria in pregnancy, we further compared concentrations of these factors in blood between malaria-infected and uninfected pregnancies.

          Methodology/Principal Findings

          We measured trophoblast invasion, migration and viability in response to treatment with serum or plasma from two independent cohorts of Papua New Guinean women infected with Plasmodium falciparum or Plasmodium vivax in early pregnancy. Compared to uninfected women, serum and plasma from women with P. falciparum reduced trophoblast invasion (P = .06) and migration (P = .004). P. vivax infection did not alter trophoblast migration (P = .64). The P. falciparum-specific negative effect on placental development was independent of trophoblast viability, but associated with high-density infections. Serum from P. falciparum infected women tended to have lower levels of trophoblast invasion promoting hormones and factors and higher levels of invasion-inhibitory inflammatory factors.

          Conclusion/Significance

          We demonstrate that in vitro models of placental development can be adapted to indirectly study the impact of malaria in early pregnancy. These infections could result in impaired trophoblast invasion with reduced transformation of maternal spiral arteries due to maternal hormonal and inflammatory disturbances, which may contribute to FGR by limiting the delivery of maternal blood to the placenta. Future prevention strategies for malaria in pregnancy should include protection in the first half of pregnancy.

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          Endovascular trophoblast invasion: implications for the pathogenesis of intrauterine growth retardation and preeclampsia.

          Peter Kaufmann, Simon Black, Berthold Huppertz (2003)
          Maternal uteroplacental blood flow increases during pregnancy. Altered uteroplacental blood flow is a core predictor of abnormal pregnancy. Normally, the uteroplacental arteries are invaded by endovascular trophoblast and remodeled into dilated, inelastic tubes without maternal vasomotor control. Disturbed remodeling is associated with maintenance of high uteroplacental vascular resistance and intrauterine growth restriction (IUGR) and preeclampsia. Herein, we review routes, mechanisms, and control of endovascular trophoblast invasion. The reviewed data suggest that endovascular trophoblast invasion involves a side route of interstitial invasion. Failure of vascular invasion is preceded by impaired interstitial trophoblast invasion. Extravillous trophoblast synthesis of nitric oxide is discussed in relation to arterial dilation that paves the way for endovascular trophoblast. Moreover, molecular mimicry of invading trophoblast-expressing endothelial adhesion molecules is discussed in relation to replacement of endothelium by trophoblast. Also, maternal uterine endothelial cells actively prepare endovascular invasion by expression of selectins that enable trophoblast to adhere to maternal endothelium. Finally, the mother can prevent endovascular invasion by activated macrophage-induced apoptosis of trophoblast. These data are partially controversial because of methodological restrictions associated with limitations of human tissue investigations and animal studies. Animal models require special care when extrapolating data to the human due to extreme species variations regarding trophoblast invasion. Basal plates of delivered placentas or curettage specimens have been used to describe failure of trophoblast invasion associated with IUGR and preeclampsia; however, they are unsuitable for these kinds of studies, since they do not include the area of pathogenic events, i.e., the placental bed.
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            Malaria in pregnancy: pathogenesis and immunity.

            Stephen Rogerson, Lars Hviid, Patrick Duffy … (2007)
            Understanding of the biological basis for susceptibility to malaria in pregnancy was recently advanced by the discovery that erythrocytes infected with Plasmodium falciparum accumulate in the placenta through adhesion to molecules such as chondroitin sulphate A. Antibody recognition of placental infected erythrocytes is dependent on sex and gravidity, and could protect from malaria complications. Moreover, a conserved parasite gene-var2csa-has been associated with placental malaria, suggesting that its product might be an appropriate vaccine candidate. By contrast, our understanding of placental immunopathology and how this contributes to anaemia and low birthweight remains restricted, although inflammatory cytokines produced by T cells, macrophages, and other cells are clearly important. Studies that unravel the role of host response to malaria in pathology and protection in the placenta, and that dissect the relation between timing of infection and outcome, could allow improved targeting of preventive treatments and development of a vaccine for use in pregnant women.
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              Evidence for immune cell involvement in decidual spiral arteriole remodeling in early human pregnancy.

              Samantha D Smith, Caroline E Dunk, John D. Aplin … (2009)
              Decidual artery remodeling is essential for a healthy pregnancy. This process involves loss of vascular smooth muscle cells and endothelium, which are replaced by endovascular trophoblasts (vEVTs) embedded in fibrinoid. Remodeling is impaired during pre-eclampsia, a disease of pregnancy that results in maternal and fetal mortality and morbidity. Early vascular changes occur in the absence of vEVTs, suggesting that another cell type is involved; evidence from animal models indicates that decidual leukocytes play a role. We hypothesized that leukocytes participate in remodeling through the triggering of apoptosis or extracellular matrix degradation. Decidua basalis samples (8 to 12 weeks gestation) were examined by immunohistochemistry to elucidate associations between leukocytes, vEVTs, and key remodeling events. Trophoblast-independent and -dependent phases of remodeling were identified. Based on a combination of morphological attributes, vessel profiles were classified into a putative temporal series of four stages. In early stages of remodeling, vascular smooth muscle cells showed dramatic disruption and disorganization before vEVT presence. Leukocytes (identified as uterine natural killer cells and macrophages) were apparent infiltrating vascular smooth muscle cells layers and were matrix metalloproteinase-7 and -9 immunopositive. A proportion of vascular smooth muscle cells and endothelial cells were terminal deoxynucleotidyl transferase dUTP nick-end labeling positive, suggesting remodeling involves apoptosis. We thus confirm that vascular remodeling occurs in distinct trophoblast-independent and -dependent stages and provide the first evidence of decidual leukocyte involvement in trophoblast-independent stages.
              Article 0 comments Cited 130 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Lars Hviid: Role: Editor
                Journal
                Journal ID (nlm-ta): PLoS One
                Journal ID (iso-abbrev): PLoS ONE
                Journal ID (publisher-id): plos
                Journal ID (pmc): plosone
                Title: PLoS ONE
                Publisher: Public Library of Science (San Francisco, USA )
                ISSN (Electronic): 1932-6203
                Publication date Collection: 2013
                Publication date (Electronic): 31 January 2013
                Volume: 8
                Issue: 1
                Electronic Location Identifier: e55269
                Affiliations
                [1 ]Department of Medicine, University of Melbourne, Melbourne, Victoria, Australia
                [2 ]Vector Borne Disease Unit, Papua New Guinea Institute of Medical Research, Goroka, Southern Highlands Province, Papua New Guinea
                [3 ]Institute for Glycomics, Griffith University, Southport, Queensland, Australia
                [4 ]Infection and Immunity Division, Walter and Eliza Hall Institute, Parkville, Victoria, Australia
                [5 ]Center for Global Health, Case Western Reserve University, Cleveland, Ohio, United States of America
                [6 ]Center for Immunology, Macfarlane Burnet Institute of Medical Research and Public Health, Melbourne, Victoria, Australia
                [7 ]Barcelona Center for International Health, University of Barcelona, Barcelona, Spain
                [8 ]Maternal and Fetal Health Research Centre, Institute of Human Development, University of Manchester, Manchester, United Kingdom
                [9 ]St. Mary's Hospital, Central Manchester University Hospitals NHS Foundation Trust, Manchester Academic Health Science Centre, Manchester, United Kingdom
                University of Copenhagen, Denmark
                Author notes

                Competing Interests: The authors have declared that no competing interests exist.

                Manuscript revision: AU DS MO RW SH HU LR EL IM CK JB PS JA JG SR. Conceived and designed the experiments: AU SR. Performed the experiments: AU JA JG DS. Analyzed the data: AU JB JA JG SR. Contributed reagents/materials/analysis tools: DS MO RW SH HU LR EL FB IM CK JB PS SR. Wrote the paper: AU JG SR.

                Article
                Publisher ID: PONE-D-12-07749
                DOI: 10.1371/journal.pone.0055269
                PMC ID: 3561386
                PubMed ID: 23383132
                SO-VID: b2465c5f-d131-44a6-adc3-5595d02a3484
                Copyright statement: Copyright @ 2013
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                Date received : 15 March 2012
                Date accepted : 29 December 2012
                Page count
                Pages: 10
                Funding
                This project was supported by the NHMRC (Project Grant 509185 to SJR and Project Grant 575534 to JB and SR). JB was supported by an Australian Research Council Future Fellowship. Travel costs of AJU to Manchester University were supported by the Australian Society for Medical Research International Research Award, and the Australian Society for Parasitology Researcher Exchange Award. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
                Categories
                Subject: Research Article
                Subject: Biology
                Subject: Developmental Biology
                Subject: Molecular Development
                Subject: Medicine
                Subject: Endocrinology
                Subject: Reproductive Endocrinology
                Subject: Infectious Diseases
                Subject: Parasitic Diseases
                Subject: Malaria
                Subject: Plasmodium Falciparum
                Subject: Tropical Diseases (Non-Neglected)
                Subject: Malaria
                Subject: Obstetrics and Gynecology
                Subject: Pregnancy
                Subject: Pregnancy Complications

                ScienceOpen disciplines: Uncategorized
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                ScienceOpen disciplines: Uncategorized

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