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The role of inflammasome in the control and pathogenesis of leishmaniasis caused by Leishmania amazonensis and its relation with disease severity in resistant or susceptible hosts

Grant number: 15/10378-6
Support Opportunities:Scholarships in Brazil - Doctorate
Effective date (Start): August 01, 2015
Effective date (End): August 26, 2019
Field of knowledge:Biological Sciences - Immunology - Cellular Immunology
Acordo de Cooperação: Coordination of Improvement of Higher Education Personnel (CAPES)
Principal Investigator:Dario Simões Zamboni
Grantee:Gustavo Fernando da Silva Quirino
Host Institution: Faculdade de Medicina de Ribeirão Preto (FMRP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil
Associated research grant:14/04684-4 - The inflammasome in the host response against intracellular pathogens and the microbial mechanisms for its evasion, AP.TEM
Associated scholarship(s):18/03318-5 - Assessing the role of Caspase-8 in the inflammasome, BE.EP.DR


Leishmania amazonensis is the causative agent of American Tegumentary Leishmaniasis in Brasil. The infected individuals can develop several types of the disease, such as benign forms presenting localized lesions that spontaneously heal (Localized cutaneous Leishmaniasis - LCL), the diffuse form of disease, characterized by high parasite numbers in non-ulcerated lesions (Diffuse cutaneous Leishmaniasis - DCL) or mucocutaneous leishmaniasis, that can destroy the oral and nasal cavities. The role of innate immunity, particularly the Nod-like receptors (NLRs) during Leishmania infection is not fully understood. Recently, we showed that NLRP3, an inflammasome activator receptor that trigger IL-1b secretion is related to L. amazonensis control in resistant C57BL/6 mice. However, it has also been demonstrated that inflammasome activation can lead to disease susceptibility during L. major infection of susceptible BALB/c mice. Thus, the hypothesis of this project is that inflammasome activation can determine the course of protective or deleterious immune responses during L. amazonensis infection, depending upon the host genetic background. It is possible that inflammasome activation in susceptible hosts trigger pathways leading to severe forms of the disease, such as DCL. In contrast, in the resistant host, inflammasome activation leads to benign forms, such as LCL. Moreover, this work will also evaluate the role of other inflammasome receptors, such as NLRP6 and NLRP12 during L. amazonensis infection. Finally, it will also be evaluated the mechanisms that cooperate with inflammasome, such as autophagy, and its role in the control of L. amazonensis infection. The development of this work will increase the knowledge about molecules and mechanisms related to host resistance or susceptibility to infection, establishing possible markers and new targets for future therapies against the disease. (AU)

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Scientific publications
(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)
DAS GRACAS CORSI-ZUELLI, FABIANA MARIA; BROGNARA, FERNANDA; DA SILVA QUIRINO, GUSTAVO FERNANDO; HIROKI, CARLOS HIROJI; FAIS, RAFAEL SOBRANO; DEL-BEN, CRISTINA MARTA; ULLOA, LUIS; SALGADO, HELIO CESAR; KANASHIRO, ALEXANDRE; LOUREIRO, CAMILA MARCELINO. Neuroimmune Interactions in Schizophrenia: Focus on Vagus Nerve Stimulation and Acetylcholine the Alpha-7 nicotinic Acetylcholine Receptor. FRONTIERS IN IMMUNOLOGY, v. 8, . (12/05178-0, 16/12195-9, 13/20549-7, 11/20343-4, 16/07641-0, 16/11988-5, 15/10378-6)

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