Plasma-derived extracellular vesicles from Plasmodium vivax patients signal spleen fibroblasts via NF-kB facilitating parasite cytoadherence

Nat Commun. 2020 Jun 2;11(1):2761. doi: 10.1038/s41467-020-16337-y.

Abstract

Plasmodium vivax is the most widely distributed human malaria parasite. Previous studies have shown that circulating microparticles during P. vivax acute attacks are indirectly associated with severity. Extracellular vesicles (EVs) are therefore major components of circulating plasma holding insights into pathological processes. Here, we demonstrate that plasma-derived EVs from Plasmodium vivax patients (PvEVs) are preferentially uptaken by human spleen fibroblasts (hSFs) as compared to the uptake of EVs from healthy individuals. Moreover, this uptake induces specific upregulation of ICAM-1 associated with the translocation of NF-kB to the nucleus. After this uptake, P. vivax-infected reticulocytes obtained from patients show specific adhesion properties to hSFs, reversed by inhibiting NF-kB translocation to the nucleus. Together, these data provide physiological EV-based insights into the mechanisms of human malaria pathology and support the existence of P. vivax-adherent parasite subpopulations in the microvasculature of the human spleen.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Adhesion
  • Cell-Derived Microparticles
  • Disease Models, Animal
  • Extracellular Vesicles / metabolism*
  • Extracellular Vesicles / parasitology
  • Fibroblasts / metabolism*
  • Fibroblasts / pathology
  • Host-Parasite Interactions / physiology
  • Humans
  • Intercellular Adhesion Molecule-1 / metabolism
  • Malaria, Vivax / parasitology
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Microvessels / parasitology
  • NF-kappa B / metabolism*
  • Plasma*
  • Plasmodium vivax / physiology*
  • Proteomics
  • Reticulocytes / metabolism*
  • Reticulocytes / parasitology
  • Spleen / metabolism*
  • Spleen / pathology

Substances

  • ICAM1 protein, human
  • NF-kappa B
  • Intercellular Adhesion Molecule-1