The role of NLRP3 and AIM2 in inflammasome activation during Brucella abortus infection

Autores
Marin, Fernanda M.; Franco, Miriam M. Costa; Gomez, Marco Tulio R.; Miraglia, Maria Cruz; Giambartolomei, Guillermo Hernan; Oliveira, Sergio C.
Año de publicación
2017
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
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.
Fil: Marin, Fernanda M.. Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas; Brasil
Fil: Franco, Miriam M. Costa. Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas; Brasil
Fil: Gomez, Marco Tulio R.. Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas; Brasil
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
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
Fil: Oliveira, Sergio C.. Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas; Brasil
Materia
Inflammasome
Dendritic Cells
Aim2
Nlrp3
Neurobrucellosis
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/47417
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/47417
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling The role of NLRP3 and AIM2 in inflammasome activation during Brucella abortus infectionMarin, Fernanda M.Franco, Miriam M. CostaGomez, Marco Tulio R.Miraglia, Maria CruzGiambartolomei, Guillermo HernanOliveira, Sergio C.InflammasomeDendritic CellsAim2Nlrp3Neurobrucellosishttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3The 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.Fil: Marin, Fernanda M.. Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas; BrasilFil: Franco, Miriam M. Costa. Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas; BrasilFil: Gomez, Marco Tulio R.. Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas; BrasilFil: 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; ArgentinaFil: 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; ArgentinaFil: Oliveira, Sergio C.. Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas; BrasilSpringer2017-02info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/47417Marin, 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; 215-2231863-2297CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1007/s00281-016-0581-1info:eu-repo/semantics/altIdentifier/url/https://link.springer.com/article/10.1007%2Fs00281-016-0581-1info:eu-repo/semantics/altIdentifier/url/https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5233600/info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T09:46:16Zoai:ri.conicet.gov.ar:11336/47417instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-03 09:46:17.115CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv The role of NLRP3 and AIM2 in inflammasome activation during Brucella abortus infection
title The role of NLRP3 and AIM2 in inflammasome activation during Brucella abortus infection
spellingShingle The role of NLRP3 and AIM2 in inflammasome activation during Brucella abortus infection
Marin, Fernanda M.
Inflammasome
Dendritic Cells
Aim2
Nlrp3
Neurobrucellosis
title_short The role of NLRP3 and AIM2 in inflammasome activation during Brucella abortus infection
title_full The role of NLRP3 and AIM2 in inflammasome activation during Brucella abortus infection
title_fullStr The role of NLRP3 and AIM2 in inflammasome activation during Brucella abortus infection
title_full_unstemmed The role of NLRP3 and AIM2 in inflammasome activation during Brucella abortus infection
title_sort The role of NLRP3 and AIM2 in inflammasome activation during Brucella abortus infection
dc.creator.none.fl_str_mv Marin, Fernanda M.
Franco, Miriam M. Costa
Gomez, Marco Tulio R.
Miraglia, Maria Cruz
Giambartolomei, Guillermo Hernan
Oliveira, Sergio C.
author Marin, Fernanda M.
author_facet Marin, Fernanda M.
Franco, Miriam M. Costa
Gomez, Marco Tulio R.
Miraglia, Maria Cruz
Giambartolomei, Guillermo Hernan
Oliveira, Sergio C.
author_role author
author2 Franco, Miriam M. Costa
Gomez, Marco Tulio R.
Miraglia, Maria Cruz
Giambartolomei, Guillermo Hernan
Oliveira, Sergio C.
author2_role author
author
author
author
author
dc.subject.none.fl_str_mv Inflammasome
Dendritic Cells
Aim2
Nlrp3
Neurobrucellosis
topic Inflammasome
Dendritic Cells
Aim2
Nlrp3
Neurobrucellosis
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv 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.
Fil: Marin, Fernanda M.. Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas; Brasil
Fil: Franco, Miriam M. Costa. Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas; Brasil
Fil: Gomez, Marco Tulio R.. Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas; Brasil
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
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
Fil: Oliveira, Sergio C.. Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas; Brasil
description 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.
publishDate 2017
dc.date.none.fl_str_mv 2017-02
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/47417
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
1863-2297
CONICET Digital
CONICET
url http://hdl.handle.net/11336/47417
identifier_str_mv 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
1863-2297
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.1007/s00281-016-0581-1
info:eu-repo/semantics/altIdentifier/url/https://link.springer.com/article/10.1007%2Fs00281-016-0581-1
info:eu-repo/semantics/altIdentifier/url/https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5233600/
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
application/pdf
application/pdf
dc.publisher.none.fl_str_mv Springer
publisher.none.fl_str_mv Springer
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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