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dc.contributor.author Marin, Fernanda M.
dc.contributor.author Franco, Miriam M. Costa
dc.contributor.author Gomez, Marco Tulio R.
dc.contributor.author Miraglia, Maria Cruz
dc.contributor.author Giambartolomei, Guillermo Hernan
dc.contributor.author Oliveira, Sergio C.
dc.date.available 2018-06-05T21:05:46Z
dc.date.issued 2017-02
dc.identifier.citation Marin, Fernanda M.; Franco, Miriam M. Costa; Gomez, Marco Tulio R.; Miraglia, Maria Cruz; Giambartolomei, Guillermo Hernan; et al.; The role of NLRP3 and AIM2 in inflammasome activation during Brucella abortus infection; Springer; Seminars in Immunopathology; 39; 2; 2-2017; 215-223
dc.identifier.issn 1863-2297
dc.identifier.uri http://hdl.handle.net/11336/47417
dc.description.abstract The innate immune system is essential for the detection and elimination of Bacterial pathogens. Upon inflammasome activation, caspase-1 cleaves pro-IL-1β and pro-IL-18 to their mature forms IL-1β and IL-18, respectively, and the cell undergoes inflammatory death termed pyroptosis. Here, we reviewed recent findings demonstrating that Brucella abortus ligands activate NLRP3 and AIM2 inflammasomes which lead to control of infection. This protective effect is due to the inflammatory response caused by IL-1β and IL-18 rather than cell death. Brucella DNA is sensed by AIM2 and bacteria-induced mitochondrial reactiveoxygen species is detected by NLRP3. However, deregulation of pro-inflammatory cytokine production can lead to immunopathology. Nervous system invasion by bacteria of the genus Brucella results in an inflammatory disorder termedneurobrucellosis. Herein, we discuss the mechanism of caspase-1 activation and IL-1β secretion in glial cells infected with B. abortus.Our results demonstrate that the ASC inflammasome is indispensable for inducing the activation of caspase-1 and secretion of IL-1β upon infection of astrocytes and microglia with Brucella. Moreover, our results demonstrate that secretion of IL-1β by Brucella-infected glial cells depends on NLRP3 and AIM2 and leads to neurobrucellosis. Further, the inhibition of the host cell inflammasome as an immune evasion strategy has been described for bacterial pathogens. We discuss here that the bacterial type IV secretion system VirB is required for inflammasome activation in host cells during infection. Taken together, our results indicate that Brucella is sensed by ASC inflammasomes mainly NLRP3 andAIM2 that collectively orchestrate a robust caspase-1 activation and pro-inflammatory response.
dc.format application/pdf
dc.language.iso eng
dc.publisher Springer
dc.rights info:eu-repo/semantics/restrictedAccess
dc.rights.uri https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject INFLAMMASOME
dc.subject DENDRITIC CELLS
dc.subject AIM2
dc.subject NLRP3
dc.subject NEUROBRUCELLOSIS
dc.subject.classification Inmunología
dc.subject.classification Medicina Básica
dc.subject.classification CIENCIAS MÉDICAS Y DE LA SALUD
dc.title The role of NLRP3 and AIM2 in inflammasome activation during Brucella abortus infection
dc.type info:eu-repo/semantics/article
dc.type info:ar-repo/semantics/artículo
dc.type info:eu-repo/semantics/publishedVersion
dc.date.updated 2018-06-05T20:13:02Z
dc.journal.volume 39
dc.journal.number 2
dc.journal.pagination 215-223
dc.journal.pais Alemania
dc.journal.ciudad Berlín
dc.description.fil Fil: Marin, Fernanda M.. Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas; Brasil
dc.description.fil Fil: Franco, Miriam M. Costa. Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas; Brasil
dc.description.fil Fil: Gomez, Marco Tulio R.. Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas; Brasil
dc.description.fil Fil: Miraglia, Maria Cruz. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina
dc.description.fil Fil: Giambartolomei, Guillermo Hernan. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina
dc.description.fil Fil: Oliveira, Sergio C.. Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas; Brasil
dc.journal.title Seminars in Immunopathology
dc.relation.alternativeid info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1007/s00281-016-0581-1
dc.relation.alternativeid info:eu-repo/semantics/altIdentifier/url/https://link.springer.com/article/10.1007%2Fs00281-016-0581-1
dc.conicet.fuente unificacion


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info:eu-repo/semantics/restrictedAccess Excepto donde se diga explícitamente, este item se publica bajo la siguiente descripción: Creative Commons Attribution-NonCommercial-ShareAlike 2.5 Unported (CC BY-NC-SA 2.5)