Atorvastatin prevents Plasmodium falciparum cytoadherence and endothelial damage
- Equal contributors
1 INSERM, UMR S945, Université Pierre et Marie Curie-Paris 6, CHU-Pitié-Salpêtrière, 91 bd de l'Hôpital, 75013 Paris, France
2 INSERM, UMR S525, Université Pierre et Marie Curie-Paris 6, Paris, France
3 AP-HP, Groupe hospitalier Pitié-Salpêtrière, Service Parasitologie-Mycologie, Paris, France
4 Okinawa Institute of Science and Technology, Onna, Okinawa, Japan
5 Department of Microbiology and Molecular Medicine, University of Geneva, Geneva, Switzerland
6 Institut Pierre Richet/Institut National de la Sante Publique, Abidjan, Ivory Coast
Malaria Journal 2011, 10:52 doi:10.1186/1475-2875-10-52Published: 28 February 2011
The adhesion of Plasmodium falciparum parasitized red blood cell (PRBC) to human endothelial cells (EC) induces inflammatory processes, coagulation cascades, oxidative stress and apoptosis. These pathological processes are suspected to be responsible for the blood-brain-barrier and other organs' endothelial dysfunctions observed in fatal cases of malaria. Atorvastatin, a drug that belongs to the lowering cholesterol molecule family of statins, has been shown to ameliorate endothelial functions and is widely used in patients with cardiovascular disorders.
The effect of this compound on PRBC induced endothelial impairments was assessed using endothelial co-culture models.
Atorvastatin pre-treatment of EC was found to reduce the expression of adhesion molecules and P. falciparum cytoadherence, to protect cells against PRBC-induced apoptosis and to enhance endothelial monolayer integrity during co-incubation with parasites.
These results might suggest a potential interest use of atorvastatin as a protective treatment to interfere with the pathophysiological cascades leading to severe malaria.