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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

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

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Author(s):
Matteucci, Kely C. [1, 2] ; Pereira, Gustavo J. S. [3] ; Weinlich, Ricardo [4] ; Bortoluci, Karina R. [1, 2]
Total Authors: 4
Affiliation:
[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
Total Affiliations: 4
Document type: Journal article
Source: Journal of Leukocyte Biology; v. 106, n. 3, SI, p. 531-540, SEP 2019.
Web of Science Citations: 4
Abstract

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)

FAPESP's process: 17/25942-0 - Cross talk between RIP3K and NLRP3 during T. cruzi infection
Grantee:Karina Ramalho Bortoluci
Support Opportunities: Regular Research Grants
FAPESP's process: 15/18003-1 - Interaction between autophagy and pattern recognition receptors to the control of Trypanosoma Cruzi infection
Grantee:Karina Ramalho Bortoluci
Support Opportunities: Regular Research Grants