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Interaction between autophagy and pattern recognition receptors to the control of Trypanosoma Cruzi infection

Grant number: 15/18003-1
Support Opportunities:Regular Research Grants
Duration: July 01, 2016 - June 30, 2018
Field of knowledge:Biological Sciences - Immunology - Cellular Immunology
Principal Investigator:Karina Ramalho Bortoluci
Grantee:Karina Ramalho Bortoluci
Host Institution: Centro de Terapia Celular e Molecular. Universidade Federal de São Paulo (UNIFESP). Campus São Paulo. São Paulo , SP, Brazil
Associated researchers:Soraya Soubhi Smaili


Autophagy is a homeostatic process by which misfolded proteins and damaged organelles are degraded. Autophagy also contibutes to degrade macromolecules under starvation. In infectious processes, autophagy helps to control microorganisms by deliverying them to degradation in autolysosomes. Pattern recognition receptors (PRRs) have been related to the regulation of autophagy. Toll-like receptors (TLRs) activate the process of autophagy, whereas the role inflammasomes is controversial and remains to be elucidated. Since both TLRs and inflammassomes are involved in the control of Trypanosoma cruzi (T. cruzi), the present proposal aims to elucidate the role of autophagy in host resistance against T. cruzi and to uncover molecular mechanisms mediated by PRRs to regulate this process. (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)
BUZZO, CARINA DE LIMA; MEDINA, TIAGO; BRANCO, LAURA M.; LAGE, SILVIA L.; DE SOUZA FERREIRA, LUIS CARLOS; AMARANTE-MENDES, GUSTAVO P.; HOTTIGER, MICHAEL O.; DE CARVALHO, DANIEL D.; BORTOLUCI, KARINA R.. Epigenetic regulation of nitric oxide synthase 2, inducible (Nos2) by NLRC4 inflammasomes involves PARP1 cleavage. SCIENTIFIC REPORTS, v. 7, . (15/18003-1, 13/16010-5)
MATTEUCCI, KELY C.; PEREIRA, GUSTAVO J. S.; WEINLICH, RICARDO; BORTOLUCI, KARINA R.. Frontline Science: Autophagy is a cell autonomous effector mechanism mediated by NLRP3 to control Trypanosoma cruzi infection. Journal of Leukocyte Biology, v. 106, n. 3, SI, p. 531-540, . (17/25942-0, 15/18003-1)

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