Efeitos in vivo e in vitro da lectina de Synadenium carinatum sobre a infecção murina por Leishmania (Leishmania) amazonensis

Abstract

Introduction: Leishmaniasis are illnesses caused by protozoan of the genus Leishmania, intracellular parasites of macrophages, that appears under diverse clinical forms. The cellular immune response is the effective protective response against these intracellular parasites. Lectins are capable to induce the production, by murine mononuclear cells, of interferon gamma (IFN - γ ), IL-12 and TNF-α, important molecules in an immune response for a Th1 profile, required to control this parasitism. O bjectives: To analyze the biological effect of the latex lectin of the Synadenium carinatum (ScLL), associate or not to the soluble Leishmania antigen (SLA), on the murine infection by L. (L.) amazonensis, evaluating its immunostimulating profile in cutaneous lesions and in infected macrophages. Materials and Methods: To evaluate the adjuvant potential of ScLL, groups of five mice had been immunized with different concentrations of this lectin associated or not to SLA. The infection of these animals was monitored weekly by measuring the infected paw during 10 weeks, when were evaluated the cellular and humoral immune responses through DTH and ELISA, respectively, as well as the expression of the IFN-γ, IL-4, IL-12, TNF-α and iNOS cytokines in the place of the lesion. The immunostimulating effect of ScLL was evaluated in culture of murine peritoneal macrophages stimulated with this lectin after 24, 48 and 72 hours of infection by L (L.) amazonensis, when the culture supernatants were harvested for the determination of NO and IL-12 production. The genic expression of cytokines as IL-1β, IL-12, TNF- α and iNOS and the intracellular parasitic load were analyzed 24, 48 and 72 hours after infection. Results: The ScLL lectin, in the concentration of 10 μg/ml was capable to stimulate the expression of IL-1β, TNF-α and iNOS cytokines, in vitro, as well as reducing in a significant way, the proliferation of parasites in the interior of macrophages. In vivo, this lectin was capable to protect the immunized mice partially, controlling the development of the lesion and inducing the expression of IFN-γ, IL-12, TNF-α and iNOS cytokines. High levels of IgG2a and low levels of IgG1 were detected in the serum of the immunized animals, being correlated with the control of the infection. Conclusions: The ScLL lectin conferred partial protection to the animals immunized after challenge with L. (L.) amazonensis, inducing a profile of immune response capable to control the parasitism in vivo e in vitro. Jointly, the data obtained with ScLL suggests that it can be used as adjuvant in experimental models of vaccination against L. (L.) amazonensis.