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(Referência obtida automaticamente do Web of Science, por meio da informação sobre o financiamento pela FAPESP e o número do processo correspondente, incluída na publicação pelos autores.)

Frontline Science: Autophagy is a cell autonomous effector mechanism mediated by NLRP3 to control Trypanosoma cruzi infection

Texto completo
Autor(es):
Matteucci, Kely C. [1, 2] ; Pereira, Gustavo J. S. [3] ; Weinlich, Ricardo [4] ; Bortoluci, Karina R. [1, 2]
Número total de Autores: 4
Afiliação do(s) autor(es):
[1] Univ Fed Sao Paulo, Dept Ciencias Biol, Sao Paulo - Brazil
[2] Univ Fed Sao Paulo, Ctr Terapia Celular & Mol CTC Mol, Sao Paulo - Brazil
[3] Univ Fed Sao Paulo, Dept Farmacol INFAR, Sao Paulo - Brazil
[4] Hosp Israelita Albert Einstein, Inst Ensino & Pesquisa, Sao Paulo - Brazil
Número total de Afiliações: 4
Tipo de documento: Artigo Científico
Fonte: Journal of Leukocyte Biology; v. 106, n. 3, SI, p. 531-540, SEP 2019.
Citações Web of Science: 4
Resumo

Autophagy and inflammasome activation are cell-autonomous and cross-regulated processes involved in host resistance against infections. Our group previously described that NLRP3 inflammasome is required for the control of Trypanosoma cruzi, the causative agent of Chagas disease. However, the involvement of autophagy in this process was unclear. Here, we demonstrated that T. cruzi was able to induce an increase in LC3-II expression as well as autophagosome and autolysosome formation in peritoneal macrophages (PMs) from C57BL/6 wild-type mice. Moreover, the pharmacologic inhibition of autophagic machinery impaired the ability of PMs to control T. cruzi replication. Importantly, NLRP3 was required for the induction of a regular autophagic flux in response to T. cruzi, an effect mediated by its participation in the autolysosomes formation. Together, these results indicate autophagy as an effector mechanism mediated by NLRP3 to control T. cruzi infection. (AU)

Processo FAPESP: 17/25942-0 - Interação entre as vias mediadas por RIP3K e NLRP3 na infecção pelo Trypanosoma cruzi
Beneficiário:Karina Ramalho Bortoluci
Modalidade de apoio: Auxílio à Pesquisa - Regular
Processo FAPESP: 15/18003-1 - Interação entre autofagia e receptores da imunidade inata para o controle da infecção pelo Trypanosoma cruzi
Beneficiário:Karina Ramalho Bortoluci
Modalidade de apoio: Auxílio à Pesquisa - Regular