Interleukin-3-deficient mice have increased susceptibility to Plasmodium berghei infection (56.2)

Abstract

Interleukin-3 (IL-3), which can be derived from T cells and other sources, is well documented at promoting the in vitro differentiation and proliferation of murine hematopoietic progenitors, yielding multipotential blast cells, mast cells, and mature cells of the myeloid and erythroid lineages. Although IL-3-deficient (knockout [KO]) mice display intact steady-state hematopoiesis, administration of IL-3 to mice and humans can promote hematopoiesis and influence the effector functions of mature hematopoietic cells in vivo. Because of these biological activities of IL-3, the contribution of IL-3 to resistance to blood-stage malaria was investigated by infecting KO mice intraperitoneally with Plasmodium berghei-infected RBCs. We found that KO mice were more susceptible to infection than wild-type (WT) mice, as evidenced by markedly higher peak parasitemia. P. berghei-infected KO mice also had significantly greater anemia and splenomegaly compared to similarly infected WT mice. Our results indicate that IL-3 contributes to resistance to P. berghei infection.