Leishmaniasis is a chronic disease that causes cutaneous or visceral manifestations, and may be lethal to humans. It is transmitted by the bite of sandflies containing the promastigote forms of parasites from the genus Leishmania. The experimental infection of BALB/c mice with L. major is characterized by skin lesions accompanied by progressive and uncontrolled proliferation of the parasite that disseminates to internal organs and leads death of the host. The susceptibility observed in this model is associated with the development of type Th2 immune responses. By contrast, resistant C57Bl/6 mice develop Th1 immune response which confers protection against the infection with Leishmania. There is increasingly interest in the search for therapies designed to improve the host immune response against Leishmania, since there are no vaccines for leishmaniasis. Several studies have identified the use of immunomodulatory proteins as tools for immune system activation that results in increased resistance to some infections. Our group has demonstrated that a lectin from Paracoccidioides brasiliensis (the etiological agent of paracoccidioidomycosis) called paracoccin, with affinity to N-acetylglucosamine, induces TNF-± and nitric oxide production by murine macrophages. The administration of paracoccin to mice confers protection against P. brasiliensis infection, leading to reduced fungal burden and pulmonary lesions, which was associated to the predominant induction of a Th1 immune response with high production of IFN-³. Since BALB/c mice are susceptible to Leishmania major infection due to the development of Th2 responses, the present study aims to assess whether the prophylactic use of paracoccin confers resistance to L. major infection in these mice. For that, we will evaluate whether treatment of mice with paracoccin prior to infection is able to improve the development of Th1 responses once the mice are infected with L. major. To assess that, we will evaluate the kinetics of lesion development and parasite loads, as well as cytokine production in mice infected with L. major that were treated or not with paracoccin prior to infection.
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