Editorial: CD36: Russian roulette of host and parasites during malaria infection

Extract

The characterization of the complex interactions occurring in the tissue during infection with the protozoan parasite Plasmodium is necessary to understand and prevent malaria pathogenesis. One syndrome—ALI/ARDS—has been reported in infections with all 5 of the human Plasmodium species and is associated with an increased risk of death [1]. Although the manifestations of this phenomenon have been described extensively, the underlying mechanisms are not fully elucidated, and therefore, efficient therapeutic interventions have not yet been developed. The host scavenger receptor CD36 is thought to play a central role in malaria-induced ALI/ARDS [2], and the targeting of this molecule has been proposed as an adjunctive therapy for severe malaria [3]. The study by Lagassé et al. [4] in this issue of the Journal of Leukocyte Biology shows why, despite its importance in ALI/ARDS, CD36 may not be a good therapeutic target.

Acute lung injuries are believed to be the result of the accumulation of PEs in the pulmonary microcirculation, as it has been observed in patients with Plasmodium falciparum and Plasmodium vivax malaria [1], as well as during experimental malaria infections in mice [5]. This process, called sequestration, is brought about by the binding of parasite molecules present on the surface of PE to host receptors on endothelial cells. The accumulation of parasites in the lungs then leads to vascular obstruction, endothelial activation, and dysfunction, as well as local host inflammatory responses [5] that compromise lung function and contribute to an ARDS.