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Malaria-associated adhesion molecule activation facilitates the destruction of uninfected red blood cells

Jill J Dalimot1, Thomas R L Klei2, Boukje M Beuger1

  • 1Department of Molecular Hematology, Sanquin Research and Landsteiner Laboratory, Amsterdam, The Netherlands.

Blood Advances
|March 29, 2022
PubMed

Insights

Severe malarial anemia (SMA) is linked to uninfected red blood cells (uRBCs) accumulating in the spleen. Adhesion molecules on uRBCs mediate this adherence, contributing to anemia.

Area of Science:

  • Hematology
  • Immunology
  • Parasitology

Background:

  • Severe malarial anemia (SMA) is a primary cause of infant mortality in malaria-endemic regions.
  • Accumulation of uninfected red blood cells (uRBCs) in the spleen is a key factor contributing to SMA.

Purpose of the Study:

  • To investigate the mechanism of uRBC sequestration in the spleen during malaria.
  • To identify adhesion molecules and parasite factors involved in uRBC adherence to the splenic extracellular matrix (ECM).

Main Methods:

  • Analysis of adhesion molecule activation (Lu/BCAM, CD44) on uRBCs from in vitro cultures and malaria patients.
  • Assessment of uRBC adherence to ECM components (laminin-α5, hyaluronic acid).
  • Investigation of parasite-derived factors influencing uRBC adhesive phenotype.

Main Results:

  • Activation of Lu/BCAM and CD44 on uRBCs mediates adherence to splenic ECM components.
  • This interaction involves elevated intracellular Ca2+ and microvesicle shedding.
  • A soluble parasite factor promotes the adhesive phenotype of uRBCs, leading to splenic retention.

Conclusions:

  • Adhesion molecule activation on uRBCs facilitates their retention in the spleen via ECM interactions.
  • This novel mechanism contributes to the pathogenesis of malaria-induced anemia.
  • Targeting these adhesion pathways could offer new therapeutic strategies for SMA.

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