Platelets inhibit erythrocyte invasion by Plasmodium falciparum at physiological platelet:erythrocyte ratios.


Journal

Transfusion medicine (Oxford, England)
ISSN: 1365-3148
Titre abrégé: Transfus Med
Pays: England
ID NLM: 9301182

Informations de publication

Date de publication:
Apr 2022
Historique:
revised: 05 10 2020
received: 21 02 2020
accepted: 27 12 2020
pubmed: 15 5 2021
medline: 14 4 2022
entrez: 14 5 2021
Statut: ppublish

Résumé

To evaluate the effect of platelet:erythrocyte (P:E) ratios on Plasmodium falciparum erythrocyte invasion. Recent reports have shown that platelets are directly involved in the immune response towards P. falciparum during erythrocyte invasion. However, the literature both supports and conflicts with a role for platelets in limiting invasion. Also, the effect of platelet numbers on invasion (parasitemia) has not been thoroughly investigated. The P. falciparum strains FCR3S1.2 and W2mef were cultured with group O erythrocytes. The cultures were synchronised and supplemented with pooled platelets at P:E ratios ranging from 1:100 to 1:2. Parasitemia was measured at 40 h by flow cytometry and by microscopy of blood smears. A linear relationship was observed between reduced invasion and increased platelet numbers at P:E ratios ranging from 1:100 to 1:20. However, this effect was reversed at lower ratios (1:10-1:2). Microscopic evaluation revealed aggregation and attachment of platelets to erythrocytes, but not specifically to parasitised erythrocytes. We have shown that under physiological P:E ratios (approx. 1:10-1:40), platelets inhibited P. falciparum invasion in a dose-dependent manner. At ratios of 1:10 and below, platelets did not further increase the inhibitory effect and, although the trend was reversed, inhibition was still maintained.

Sections du résumé

OBJECTIVE OBJECTIVE
To evaluate the effect of platelet:erythrocyte (P:E) ratios on Plasmodium falciparum erythrocyte invasion.
BACKGROUND BACKGROUND
Recent reports have shown that platelets are directly involved in the immune response towards P. falciparum during erythrocyte invasion. However, the literature both supports and conflicts with a role for platelets in limiting invasion. Also, the effect of platelet numbers on invasion (parasitemia) has not been thoroughly investigated.
METHODS/MATERIALS METHODS
The P. falciparum strains FCR3S1.2 and W2mef were cultured with group O erythrocytes. The cultures were synchronised and supplemented with pooled platelets at P:E ratios ranging from 1:100 to 1:2. Parasitemia was measured at 40 h by flow cytometry and by microscopy of blood smears.
RESULTS RESULTS
A linear relationship was observed between reduced invasion and increased platelet numbers at P:E ratios ranging from 1:100 to 1:20. However, this effect was reversed at lower ratios (1:10-1:2). Microscopic evaluation revealed aggregation and attachment of platelets to erythrocytes, but not specifically to parasitised erythrocytes.
CONCLUSION CONCLUSIONS
We have shown that under physiological P:E ratios (approx. 1:10-1:40), platelets inhibited P. falciparum invasion in a dose-dependent manner. At ratios of 1:10 and below, platelets did not further increase the inhibitory effect and, although the trend was reversed, inhibition was still maintained.

Identifiants

pubmed: 33987889
doi: 10.1111/tme.12791
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

168-174

Subventions

Organisme : Avtal om läkarutbildning och forskning (ALF)
ID : ALF-4456521
Organisme : Crafoordska Stiftelsen
ID : 20151060
Organisme : Knut och Alice Wallenbergs Stiftelse
ID : 2014.0312
Organisme : Vetenskapsrådet
ID : 2019-01683
Organisme : Vetenskapsrådet
ID : 2014-71X-14251
Organisme : University of Phayao, Thailand

Informations de copyright

© 2021 The Authors. Transfusion Medicine published by John Wiley & Sons Ltd on behalf of British Blood Transfusion Society.

Références

Satchwell TJ. Erythrocyte invasion receptors for Plasmodium falciparum: new and old. Transfus Med. 2016;26(2):77-88.
Dhabangi A, Dzik WH, Idro R, et al. Blood use in sub-Saharan Africa: a systematic review of current data. Transfusion. 2019;59(7):2446-2454.
Cox D, McConkey S. The role of platelets in the pathogenesis of cerebral malaria. Cell Mol Life Sci. 2010;67(4):557-568.
Cabrera A, Neculai D, Kain KC. CD36 and malaria: friends or foes? A decade of data provides some answers. Trends Parasitol. 2014;30(9):436-444.
Peyron F, Polack B, Lamotte D, Kolodie L, Ambroise-Thomas P. Plasmodium falciparum growth inhibition by human platelets in vitro. Parasitology. 1989;99:317-322.
Kho S, Barber BE, Johar E, et al. Platelets kill circulating parasites of all major Plasmodium species in human malaria. Blood. 2018;132(12):1332-1344.
McMorran BJ, Marshall VM, de Graaf C, et al. Platelets kill intraerythrocytic malarial parasites and mediate survival to infection. Science. 2009;323(5915):797-800.
McMorran BJ, Wieczorski L, Drysdale KE, et al. Platelet factor 4 and Duffy antigen required for platelet killing of Plasmodium falciparum. Science. 2012;338(6112):1348-1351.
Gramaglia I, Velez J, Combes V, et al. Platelets activate a pathogenic response to blood-stage Plasmodium infection but not a protective immune response. Blood. 2017;129(12):1669-1679.
Moll K, Kaneko A, Scherf A, Wahlgren M. Methods in Malaria Research. Glasgow, UK: EVIMalaR; 2013.
Crosnier C, Bustamante LY, Bartholdson SJ, et al. Basigin is a receptor essential for erythrocyte invasion by Plasmodium falciparum. Nature. 2011;480(7378):534-537.
Bertagna P, Cohen S, Geiman QM, et al. Cultivation techniques for the erythrocytic stages of malaria parasites. Bull World Health Organ. 1972;47(3):357-373.
Boyle MJ, Wilson DW, Richards JS, et al. Isolation of viable Plasmodium falciparum merozoites to define erythrocyte invasion events and advance vaccine and drug development. PNAS. 2010;107(32):14378-14383.
Semple JW, Italiano JE, Freedman J. Platelets and the immune continuum. Nat Rev Immunol. 2011;11(4):264-274.
Kaneko O. Pf Clone's Origin; 1999. https://www.m.ehime-u.ac.jp/school/parasitology/eng/Strain1.htm. Accessed February 16, 2020.
Triglia T, Duraisingh MT, Good RT, Cowman AF. Reticulocyte-binding protein homologue 1 is required for sialic acid-dependent invasion into human erythrocytes by Plasmodium falciparum. Mol Microbiol. 2005;55(1):162-174.
Goel S, Palmkvist M, Moll K, et al. RIFINs are adhesins implicated in severe Plasmodium falciparum malaria. Nature Med. 2015;21(4):314-317.
Daniels G. Human Blood Groups. 3rd ed. Oxford, UK: Wiley-Blackwell; 2013.
Leffler EM, Band G, Busby GBJ, et al. Resistance to malaria through structural variation of red blood cell invasion receptors. Science. 2017;356(6343):eaam6393.

Auteurs

Philaiphon Jongruamklang (P)

Department of Laboratory Medicine, Division of Hematology and Transfusion Medicine, Lund University, Lund, Sweden.
Department of Medical Technology, School of Allied Health Sciences, University of Phayao, Phayao, Thailand.

Johan Rebetz (J)

Department of Laboratory Medicine, Division of Hematology and Transfusion Medicine, Lund University, Lund, Sweden.

Rick Kapur (R)

Department of Experimental Immunohematology, Sanquin Research, Amsterdam, The Netherlands.
Landsteiner Laboratory, Amsterdam UMC, University of Amsterdam, Amsterdam, The Netherlands.

Kristina E M Persson (KEM)

Department of Laboratory Medicine, Division of Clinical Chemistry and Pharmacology, Lund University, Lund, Sweden.
Clinical Chemistry and Pharmacology, Laboratory Medicine, Office for Medical Services, Region Skåne, Lund, Sweden.

Martin L Olsson (ML)

Department of Laboratory Medicine, Division of Hematology and Transfusion Medicine, Lund University, Lund, Sweden.
Clinical Immunology and Transfusion Medicine, Laboratory Medicine, Office for Medical Services, Region Skåne, Lund, Sweden.

John W Semple (JW)

Department of Laboratory Medicine, Division of Hematology and Transfusion Medicine, Lund University, Lund, Sweden.
Clinical Immunology and Transfusion Medicine, Laboratory Medicine, Office for Medical Services, Region Skåne, Lund, Sweden.

Jill R Storry (JR)

Department of Laboratory Medicine, Division of Hematology and Transfusion Medicine, Lund University, Lund, Sweden.
Clinical Immunology and Transfusion Medicine, Laboratory Medicine, Office for Medical Services, Region Skåne, Lund, Sweden.

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