Splenectomy portends an increased risk of severe infection, pulmonary thrombosis and (predominantly hematologic) malignancy. Reliable and handy markers of splenic functionality are lacking. A powerful way to determine the function of an organ – here the quality control performed by the spleen on the red blood cells – is to assess what happens when that organ is absent or dysfunctional. The spleen is one of the few organs that can be completely removed or that can become severely dysfunctional without immediate impact on survival. We have shown that the deformability of RBCs is slightly but significantly altered in splenectomized patients, even in those without pre-existing RBC disease. We currently develop new methods to quantify red blood cells containing vacuoles, as an optimized marker of hyposplenism.

Malaria still kills more than half million people per year all around the world, especially African children. It is caused by a protozoan parasite of the genus Plasmodium, that is transmitted to the erythrocytes by an Anopheles mosquito. The only parasitic form transmitted from the human host to the mosquito vector are the mature gametocytes. Blocking this transmission is a key asset to control the spread of malaria and eventually eradicate it, as pointed out by WHO. A functional spleen retains and clears rigid erythrocytes from the circulation. In malaria, infected erythrocytes are more stringently retained compared to non-infected erythrocytes. Mature gametocytes are deformable enough to circulate. Using the team’s expertise in splenic function and spleen-mimetic techniques, we have selected compounds that stiffen mature gametocytes, promoting their splenic retention. This drug-induced retention is expected to make them unavailable for mosquitoes, thereby blocking the transmisison of malaria.