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Interaction of Insulin-Like Growth Factor I and cytokines Th1 and Th2 in murine macrophage infection by Leishmania (Leishmania) amazonensis

Grant number: 17/02959-4
Support type:Scholarships in Brazil - Master
Effective date (Start): August 01, 2017
Effective date (End): June 30, 2019
Field of knowledge:Biological Sciences - Parasitology - Protozoology of Parasites
Principal researcher:Hiro Goto
Grantee:Fernanda Narangeira de Araujo
Home Institution: Instituto de Medicina Tropical de São Paulo (IMT). Universidade de São Paulo (USP). São Paulo , SP, Brazil

Abstract

In Leishmania infection, along with the specific immune response, nonspecific factors participate in its evolution as growth factors, including the Insulin-Like Growth Factor-I (IGF-I). In previous studies carried out by the group of Profª Drª Hiro Goto, it was demonstrated that extrinsic IGF-I acts as a promoter of proliferation and growth of parasites of the genus Leishmania and acts in the aggravation of lesions in experimental leishmaniasis. After demonstrating that intrinsic IGF-I is abundantly expressed in macrophages, in vitro experiments were performed on murine macrophages infected with Leishmania (Leishmania) major. By silencing IGF-I RNA by interference RNA, it was observed that IGF-I stimulates and/or modulates the effect of Th2 cytokines (IL-4 and IL-13) and inhibits and/or modulates Th1 cytokine (IFN-g). Data from the literature show, on the other hand, that there are peculiarities in the parasite-host-dependent interaction of the Leishmania species, with a reflection on the evolution of infection and the effects of the elements involved in the immune response. In this sense, the role of cytokines in the specific response in the expression of intrinsic IGF-I in the context of L. amazonensis infection is unknown, as is the result of the interaction of IGF-I and cytokines in the evolution of infection. Due to species-specific specificities, the studies will focus on the evaluation of IGF-I production by macrophages infected with L. amazonensis under the effect of Th1 and Th2 cytokines And the interaction of IGF-I and cytokines in the parasitism and mechanisms of its control in the macrophage. (AU)