Organotypic endothelial adhesion molecules are key for Trypanosoma brucei tropism and virulence

Mariana de Niz, Daniela Brás, Marie Ouarné, Mafalda Pedro, Ana M. Nascimento, Lenka Henao Misikova, Cláudio A. Franco, Luisa M. Figueiredo*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

23 Citations (Scopus)

Abstract

Trypanosoma brucei is responsible for lethal diseases in humans and cattle in Sub-Saharan Africa. These extracellular parasites extravasate from the blood circulation into several tissues. The importance of the vasculature in tissue tropism is poorly understood. Using intravital imaging and bioluminescence, we observe that gonadal white adipose tissue and pancreas are the two main parasite reservoirs. We show that reservoir establishment happens before vascular permeability is compromised, suggesting that extravasation is an active mechanism. Blocking endothelial surface adhesion molecules (E-selectin, P-selectins, or ICAM2) significantly reduces extravascular parasite density in all organs and delays host lethality. Remarkably, blocking CD36 has a specific effect on adipose tissue tropism that is sufficient to delay lethality, suggesting that establishment of the adipose tissue reservoir is necessary for parasite virulence. This work demonstrates the importance of the vasculature in a T. brucei infection and identifies organ-specific adhesion molecules as key players for tissue tropism.

Original languageEnglish
Article number109741
JournalCell reports
Volume36
Issue number12
DOIs
Publication statusPublished - 21 Sept 2021
Externally publishedYes

Keywords

  • Endothelial receptors
  • Intravital microscopy
  • Parasites
  • Tropism
  • Trypanosoma brucei
  • Vasculature

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