According to the World Health Organization, there are approximately 300 million to 500 million cases of malaria each year, with pregnant women and young children at highest risk. Severe anemia--a common complication of malaria--is one of the major causes of death among children.
Malaria parasites use RBCs as multiplication factories, rupturing the cells as progeny parasites exit. Infection also hampers the production of new RBCs from the bone marrow, an effect this group recently attributed to MIF, which is produced by immune cells that gobble up infected RBCs. Bucala's new study shows that mice genetically engineered to lack MIF were less anemic and survived longer than normal mice when infected with malaria-causing parasites.
The Yale team is now trying to determine whether MIF levels influence susceptibility to or severity of malarial anemia in humans. If so, synthetic inhibitors of MIF--currently in clinical development--might provide an effective alternative to the costly (and risky) blood transfusions currently used to treat malarial anemia.