Murine Malaria Parasite Sequestration: CD36 is the Major Receptor, but Cerebral Pathology is Unlinked to Sequestration

Overview

Journal Proc Natl Acad Sci U S A

Specialty Science

Date 2005 Jul 30

PMID 16051702

Citations 177

Authors

Blandine Franke-Fayard

Chris J Janse

Margarida Cunha-Rodrigues

Jai Ramesar

Philippe Buscher

Ivo Que

Clemens Lowik

Peter J Voshol

Marion A M den Boer

Sjoerd G van Duinen

Maria Febbraio

Maria M Mota

Andrew P Waters

Affiliations

Soon will be listed here.

Abstract

Sequestration of malaria-parasite-infected erythrocytes in the microvasculature of organs is thought to be a significant cause of pathology. Cerebral malaria (CM) is a major complication of Plasmodium falciparum infections, and PfEMP1-mediated sequestration of infected red blood cells has been considered to be the major feature leading to CM-related pathology. We report a system for the real-time in vivo imaging of sequestration using transgenic luciferase-expressing parasites of the rodent malaria parasite Plasmodium berghei. These studies revealed that: (i) as expected, lung tissue is a major site, but, unexpectedly, adipose tissue contributes significantly to sequestration, and (ii) the class II scavenger-receptor CD36 to which PfEMP1 can bind is also the major receptor for P. berghei sequestration, indicating a role for alternative parasite ligands, because orthologues of PfEMP1 are absent from rodent malaria parasites, and, importantly, (iii) cerebral complications still develop in the absence of CD36-mediated sequestration, dissociating parasite sequestration from CM-associated pathology. Real-time in vivo imaging of parasitic processes may be used to evaluate the molecular basis of pathology and develop strategies to prevent pathology.

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