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Background  Interleukin 32 (IL-32) is a pro-inflammatory cytokine induced in patients with American tegumentary leishmaniasis (ATL) caused by  Leishmania braziliensis . Here, we investigated whether IL-32 is also expressed in patient lesions caused by  L. amazonensis.  In addition, we evaluated experimental  L. amazonensis  and  L. braziliensis  infections in C57BL/6 transgenic mice for human IL-32γ (IL-32γTg) in comparison with wild-type (WT) mice that do not express the IL-32 gene.    Results  Human cutaneous lesions caused by  L. amazonensis  express higher levels of IL-32 than healthy control skin. In mice, the presence of IL-32γ promoted the control of cutaneous lesions caused by  L. braziliensis , but not lesions caused by  L. amazonensis  in an ear dermis infection model. In addition, IL-32γTg mice displayed less tissue parasitism and inflammation in IL-32γTg than WT mice during the healing phase of  L. braziliensis  infection. Production of antigen-specific pro-inflammatory cytokines was higher in IL-32γTg mice than in WT mice during  L. braziliensis  infection but not during  L. amazonensis  infection.    Conclusions  Human cutaneous lesions caused by  L. amazonensis  express high levels of IL-32 .  In mice, the presence of IL-32γ contributes to the lesion healing caused by  L. braziliensis  but not by  L. amazonensis . Data suggest that despite the ability for both species to induce IL-32 in humans, the connections between this cytokine and other immune players induced by related species of parasites can lead to distinct outcomes of the murine infections.

IL-32γ promotes the healing of murine cutaneous lesions caused by Leishmania braziliensis infection in contrast to Leishmania amazonensis