ArticleMalaria journal2017
Binding of Plasmodium falciparum to CD36 can be shielded by the glycocalyx.
Article in Malaria journal, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- Febrile temperature enhancesbioRxiv : the preprint server for biology · 2025Article
- PfEMP1 and var genes - Still of key importance in Plasmodium falciparum malaria pathogenesis and immunity.Advances in parasitology · 2024Review
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- Degradation of endothelial glycocalyx in Tanzanian children with falciparum malaria.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Sickle-trait hemoglobin reduces adhesion to both CD36 and EPCR by Plasmodium falciparum-infected erythrocytes.PLoS pathogens · 2021Article
- Cytoadherence Properties ofFrontiers in microbiology · 2021Article
- Unveiling the Sugary Secrets ofFrontiers in microbiology · 2021Review
- Vascular Dysfunction in Malaria: Understanding the Role of the Endothelial Glycocalyx.Frontiers in cell and developmental biology · 2021Review
- The B Subunit of PirABPathogens (Basel, Switzerland) · 2020Article
- Article
- Glycocalyx breakdown is increased in African children with cerebral and uncomplicated falciparum malaria.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Glycocalyx Breakdown Is Associated With Severe Disease and Fatal Outcome in Plasmodium falciparum Malaria.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2019Observational
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPlasmodium falciparum-infected erythrocytes sequester in the microcirculation due to interaction between surface-expressed parasite proteins and endothelial receptors. Endothelial cells are covered in a carbohydrate-rich glycocalyx that shields against undesired leukocyte adhesion. It was investigated if the cellular glycocalyx affects the binding of P. falciparum-infected erythrocytes to CD36 in vitro.
methodsGlycocalyx growth was followed in vitro by using azido sugars and cationized ferritin detecting O-glycoproteins and negatively charged proteoglycans, respectively. P. falciparum (clone FCR3/IT) was selected on Chinese hamster ovary (CHO) cells transfected with human CD36. Cytoadhesion to CHO CD36 at 1-4 days after seeding was quantified by using a static binding assay.
resultsThe glycocalyx thickness of CHO cells increased during 4 days in culture as assessed by metabolic labelling of glycans with azido sugars and with electron microscopy studying the binding of cationized ferritin to cell surfaces. The functional importance of this process was addressed in binding assays by using CHO cells transfected with CD36. In parallel with the maturation of the glycocalyx, antibody-binding to CD36 was inhibited, despite stable expression of CD36. P. falciparum selected for CD36-binding recognized CD36 on CHO cells on the first day in culture, but the binding was lost after 2-4 days.
conclusionThe endothelial glycocalyx affects parasite cytoadhesion in vitro, an effect that has previously been ignored. The previously reported loss of glycocalyx during experimental malaria may play an important role in the pathogenesis of malaria complications by allowing the close interaction between infected erythrocytes and endothelial receptors.
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