<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Hromatka BS</submitter><funding>NIAID NIH HHS</funding><pagination>154</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4070867</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>88(6)</volume><pubmed_abstract>During pregnancy, Plasmodium falciparum-infected erythrocytes cytoadhere to the placenta. Infection is likely initiated at two sites where placental trophoblasts contact maternal blood: 1) via syncytiotrophoblast (STB), a multicellular transporting and biosynthetic layer that forms the surface of chorionic villi and lines the intervillous space, and 2) through invasive cytotrophoblasts, which line uterine vessels that divert blood to the placenta. Here, we investigated mechanisms of infected erythrocyte sequestration in relationship to the microanatomy of the maternal-fetal interface. Histological analyses revealed STB denudation in placental malaria, which brought the stromal cores of villi in direct contact with maternal blood. STB denudation was associated with hemozoin deposition (P = </pubmed_abstract><journal>Biology of reproduction</journal><pubmed_title>Histopathologies, immunolocalization, and a glycan binding screen provide insights into Plasmodium falciparum interactions with the human placenta.</pubmed_title><pmcid>PMC4070867</pmcid><funding_grant_id>R21 AI079329</funding_grant_id><funding_grant_id>NIH 1R21AI079329-01A1</funding_grant_id><pubmed_authors>Hromatka BS</pubmed_authors><pubmed_authors>Niles RK</pubmed_authors><pubmed_authors>Ngeleza S</pubmed_authors><pubmed_authors>Fisher SJ</pubmed_authors><pubmed_authors>Adibi JJ</pubmed_authors><pubmed_authors>Tshefu AK</pubmed_authors></additional><is_claimable>false</is_claimable><name>Histopathologies, immunolocalization, and a glycan binding screen provide insights into Plasmodium falciparum interactions with the human placenta.</name><description>During pregnancy, Plasmodium falciparum-infected erythrocytes cytoadhere to the placenta. Infection is likely initiated at two sites where placental trophoblasts contact maternal blood: 1) via syncytiotrophoblast (STB), a multicellular transporting and biosynthetic layer that forms the surface of chorionic villi and lines the intervillous space, and 2) through invasive cytotrophoblasts, which line uterine vessels that divert blood to the placenta. Here, we investigated mechanisms of infected erythrocyte sequestration in relationship to the microanatomy of the maternal-fetal interface. Histological analyses revealed STB denudation in placental malaria, which brought the stromal cores of villi in direct contact with maternal blood. STB denudation was associated with hemozoin deposition (P = </description><dates><release>2013-01-01T00:00:00Z</release><publication>2013 Jun</publication><modification>2025-04-18T21:27:08.014Z</modification><creation>2019-03-27T01:30:52Z</creation></dates><accession>S-EPMC4070867</accession><cross_references><pubmed>23575149</pubmed><doi>10.1095/biolreprod.112.106195</doi></cross_references></HashMap>