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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.)

Inflammasome biology taught by Legionella pneumophila

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Mascarenhas, Danielle P. A. ; Zamboni, Dario S.
Total Authors: 2
Document type: Review article
Source: Journal of Leukocyte Biology; v. 101, n. 4, p. 841-849, APR 2017.
Web of Science Citations: 4

Inflammasomes are multimeric protein complexes that assemble in the cytosol of many types of cells, including innate immune cells. The inflammasomes can be activated in response to infection or in response to stress signals that induce damage in the host cell membranes. These platforms trigger inflammatory processes, cell death, and the control of microbial replication. Many inflammasomes have been described so far, including NLRP3, NAIP/NLRC4, caspase-11, and AIM2. The ligand for NLRP3 is still unidentified, but the efflux of K+ is essential for NLRP3 activation. By contrast, inflammasomes, such as those composed of NAIP/NLRC4, caspase-11, and AIM2, can be activated by bacterial flagellin, LPS, and dsDNA. The knowledge of inflammasome biology has advanced tremendously in the last decade, fostered by the use of model organisms, such as Legionella pneumophila. This bacterium evolved, infecting unicellular protozoa in freshwater environments, and the human infection is accidental. Thus, L. pneumophila did not evolve sophisticated mechanisms to inhibit mammalian innate immunity. For this reason, it has emerged as a very appropriate model of a pathogenic microbe for the investigation of inflammasome biology. In this review, we highlight the current information regarding the biology of inflammasomes and emphasize the advances achieved using L. pneumophila. We also describe the inflammasomes activated in response to L. pneumophila infection and discuss the effector mechanisms that operate to clear the infection. (AU)

FAPESP's process: 14/50268-2 - Deciphering the interactions between Legionella longbeachae and eukaryotic host cells
Grantee:Dario Simões Zamboni
Support type: Regular Research Grants
FAPESP's process: 13/08216-2 - CRID - Center for Research in Inflammatory Diseases
Grantee:Fernando de Queiroz Cunha
Support type: Research Grants - Research, Innovation and Dissemination Centers - RIDC
FAPESP's process: 14/00794-0 - Determination of the signaling pathway flagellin/NLRC 4-dependent and caspase-1/caspase-11-independent with operates in control infection caused by Legionella spp
Grantee:Danielle Pini Alves Mascarenhas
Support type: Scholarships in Brazil - Doctorate
FAPESP's process: 14/04684-4 - The inflammasome in the host response against intracellular pathogens and the microbial mechanisms for its evasion
Grantee:Dario Simões Zamboni
Support type: Research Projects - Thematic Grants