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Leishmania  infection causes diverse clinical manifestations in humans. The disease outcome is complicated by the combination of many host and parasite factors. Inbred mouse strains vary in resistance to  Leishmania major  but are highly susceptible to  Leishmania amazonensis  infection. However, rats are highly resistant to  L. amazonensis  infection due to unknown mechanisms. We use the inducible nitric oxide synthase ( Nos2)  gene knockout rat model ( Nos2  −/−  rat) to investigate the role of NOS2 against leishmania infection in rats. Our results demonstrated that diversion toward the NOS2 pathway is the key factor explaining the resistance of rats against  L. amazonensis  infection. Rats deficient in NOS2 are susceptible to  L. amazonensis  infection even though their immune response to infection is still strong. Moreover, adoptive transfer of NOS2 competent macrophages into  Nos2  −/−  rats significantly reduced disease development and parasite load. Thus, we conclude that the distinct L-arginine metabolism, observed in rat macrophages, is the basis of the strong innate resistance to  Leishmania . These data highlight that macrophages from different hosts possess distinctive properties and produce different outcomes in innate immunity to  Leishmania  infections.

Innate Resistance to Leishmania amazonensis Infection in Rat Is Dependent on NOS2