Abstract
BackgroundLeishmaniasis is a neglected vector-borne tropical disease caused by Leishmania protozoa that are transmitted to mammalian hosts by infected sand flies. Infection is associated with distinct clinical manifestations that include cutaneous, mucocutaneous and visceral lesions. Visceral leishmaniasis (VL) is the most severe form of the disease and is considered second in terms of mortality and fourth in terms of morbidity among tropical diseases. IFN-γ-producing T cells are involved in protection against the disease.MethodsCD43+/+ and CD43-/- mice on a C57BL/6 background were intravenously injected with 5 × 10 7 amastigotes of Leishmania (L.) infantum chagasi, and 30 days after infection the clinical signs of disease were examined; the splenocytes were isolated and assayed for cytokine production; and the livers were removed for phenotypic analysis of T cell subsets by flow cytometry.ResultsWe report that mice lacking CD43 display increased susceptibility to infection by Leishmania (L.) infantum chagasi, with higher parasite burdens than wild-type mice. The increased susceptibility of CD43−/− mice were associated with a weakened delayed hypersensitivity response and reduced levels of IgG2a antibodies to leishmania antigens. We further showed that expression of CD43 defines a major intrahepatic CD4+ and CD8+ T cell subsets with pro-inflammatory phenotypes and leads to increased levels of IFN-γ secretion by activated splenocytes.ConclusionsOur findings point to a role of CD43 in the development of host resistance to visceral leishmaniasis.Electronic supplementary materialThe online version of this article (doi:10.1186/s13071-015-0721-9) contains supplementary material, which is available to authorized users.
Highlights
Leishmaniasis is a neglected vector-borne tropical disease caused by Leishmania protozoa that are transmitted to mammalian hosts by infected sand flies
We used a murine model of Visceral leishmaniasis (VL) in which infection of C57BL/6 mice with Leishmania (L.) infantum chagasi amastigotes gives rise to a higher parasite load in the liver than in other organs such as the spleen and bone marrow during the first weeks, after which it is controlled by the host immune response
We observed a lower delayed-type hypersensitivity (DTH) response to the promastigote leishmania antigen in CD43−/− mice on a C57BL/6 background than in wild type C57BL/6 mice after infection with Leishmania (L.) infantum chagasi (Figure 1A). These data indicate that cellular immunity against visceral infection of leishmania parasite is impaired in knockout mice, raising the possibility that CD43 is required for optimal development of host resistance to VL
Summary
Leishmaniasis is a neglected vector-borne tropical disease caused by Leishmania protozoa that are transmitted to mammalian hosts by infected sand flies. Methods: CD43+/+ and CD43-/- mice on a C57BL/6 background were intravenously injected with 5 × 10 7 amastigotes of Leishmania (L.) infantum chagasi, and 30 days after infection the clinical signs of disease were examined; the splenocytes were isolated and assayed for cytokine production; and the livers were removed for phenotypic analysis of T cell subsets by flow cytometry. Infection with leishmania spps can induce diseases varying from local cutaneous lesions to systemic visceral manifestations. Parasites of the intracellular protozoan, Leishmania, are transmitted to mammalian hosts by sand fly vectors. IFN-γ secreted by CD4+ and CD8+ T cells mediates the respiratory burst in activated macrophages which is responsible for the production of nitric oxide needed for parasite killing inside reservoir cells [3,4].
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