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Analysis of role signaling pathways and effector molecules related to inflammasomes in the control of infection by Leishmania amazonensis


Leishmaniasis are a group of diseases to pose a major public health problem worldwide, affecting mainly less favored individuals from emerging countries. The diseases are caused by protozoan parasites of the Leishmania spp genus, presenting different known clinical forms: cutaneous, mucocutaneous and visceral. In the mammalian host these parasites preferentially infect phagocytic cells, primarily macrophages and dendritic cells of innate immune system, to which play an important role in elimination of intracellular pathogens. The Leishmania amazonensis parasite is a major etiological agent of human cutaneous leishmaniasis in the Americas, with diminished immune response in infected patients, usually developing a Th2-type response against the infection and presence of high levels of anti inflammatory cytokines, favoring the development of the infection and, therefore, the disease. These diseases are considered neglected and, despite being curable, affect around 850,000 people a year worldwide. Our group demonstrated that NLRP3 inflammasome plays an important role in the development and clinical outcome of Leishmaniasis. The inflammasome activation leads to expression of inflammatory cytokines, including IL-1² and IL-1±, which signal through the IL1R receptor. The present proposal, we intend to investigate the contribution and IL-1± and IL-1² dependent signaling pathways involved in control of infection, as well as, in release by NLRP3 independent inflammasomes, including AIM2 and NLRC4. Our results will contribute to better understanding of cellular responses associated with control of infections by Leishmania spp., as well as identify processes by which the host fights infections. (AU)

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