Glial Cell-Elicited Activation of Brain Microvasculature in Response to Brucella abortus Infection Requires ASC Inflammasome-Dependent IL-1β Production
Blood-brain barrier activation and/or dysfunction are a common feature of human neurobrucellosis, but the underlying pathogenic mechanisms are largely unknown. In this article, we describe an immune mechanism for inflammatory activation of human brain microvascular endothelial cells (HBMEC) in respo...
| Autores: | , , , , , , , , , , , , , |
|---|---|
| Tipo de recurso: | artículo |
| Estado: | Versión publicada |
| Fecha de publicación: | 2016 |
| País: | Argentina |
| Institución: | Consejo Nacional de Investigaciones Científicas y Técnicas |
| Repositorio: | CONICET Digital (CONICET) |
| Idioma: | inglés |
| OAI Identifier: | oai:ri.conicet.gov.ar:11336/23627 |
| Acceso en línea: | http://hdl.handle.net/11336/23627 |
| Access Level: | acceso abierto |
| Palabra clave: | Hbmec Brucella Neurobrucellosis Inflammasome https://purl.org/becyt/ford/3.1 https://purl.org/becyt/ford/3 |
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Glial Cell-Elicited Activation of Brain Microvasculature in Response to Brucella abortus Infection Requires ASC Inflammasome-Dependent IL-1β Production Glial Cell-Elicited Activation of Brain Microvasculature in Response to Brucella abortus Infection Requires ASC Inflammasome-Dependent IL-1β Production |
| title |
Glial Cell-Elicited Activation of Brain Microvasculature in Response to Brucella abortus Infection Requires ASC Inflammasome-Dependent IL-1β Production |
| spellingShingle |
Glial Cell-Elicited Activation of Brain Microvasculature in Response to Brucella abortus Infection Requires ASC Inflammasome-Dependent IL-1β Production Miraglia, Maria Cruz Hbmec Hbmec Brucella Brucella Neurobrucellosis Neurobrucellosis Inflammasome Inflammasome https://purl.org/becyt/ford/3.1 https://purl.org/becyt/ford/3.1 https://purl.org/becyt/ford/3 https://purl.org/becyt/ford/3 |
| title_short |
Glial Cell-Elicited Activation of Brain Microvasculature in Response to Brucella abortus Infection Requires ASC Inflammasome-Dependent IL-1β Production |
| title_full |
Glial Cell-Elicited Activation of Brain Microvasculature in Response to Brucella abortus Infection Requires ASC Inflammasome-Dependent IL-1β Production |
| title_fullStr |
Glial Cell-Elicited Activation of Brain Microvasculature in Response to Brucella abortus Infection Requires ASC Inflammasome-Dependent IL-1β Production |
| title_full_unstemmed |
Glial Cell-Elicited Activation of Brain Microvasculature in Response to Brucella abortus Infection Requires ASC Inflammasome-Dependent IL-1β Production |
| title_sort |
Glial Cell-Elicited Activation of Brain Microvasculature in Response to Brucella abortus Infection Requires ASC Inflammasome-Dependent IL-1β Production |
| dc.creator.none.fl_str_mv |
Miraglia, Maria Cruz Miraglia, Maria Cruz Franco, Miriam M. Costa Franco, Miriam M. Costa Rodríguez, Ana María Rodríguez, Ana María Bellozi, Paula M. Q. Bellozi, Paula M. Q. Ferrari, Carina Cintia Ferrari, Carina Cintia Farias, Maria Isabel Farias, Maria Isabel Dennis, Vida A. Dennis, Vida A. Barrionuevo, Paula Barrionuevo, Paula Oliveira, Antonio C. P. de Oliveira, Antonio C. P. de Pitossi, Fernando Juan Pitossi, Fernando Juan Kim, Kwang Sik Kim, Kwang Sik Delpino, María Victoria Delpino, María Victoria Oliveira, Sergio C. Oliveira, Sergio C. Giambartolomei, Guillermo Hernan Giambartolomei, Guillermo Hernan |
| author |
Miraglia, Maria Cruz |
| author_facet |
Miraglia, Maria Cruz Franco, Miriam M. Costa Rodríguez, Ana María Bellozi, Paula M. Q. Ferrari, Carina Cintia Farias, Maria Isabel Dennis, Vida A. Barrionuevo, Paula Oliveira, Antonio C. P. de Pitossi, Fernando Juan Kim, Kwang Sik Delpino, María Victoria Oliveira, Sergio C. Giambartolomei, Guillermo Hernan |
| author_role |
author |
| author2 |
Franco, Miriam M. Costa Rodríguez, Ana María Bellozi, Paula M. Q. Ferrari, Carina Cintia Farias, Maria Isabel Dennis, Vida A. Barrionuevo, Paula Oliveira, Antonio C. P. de Pitossi, Fernando Juan Kim, Kwang Sik Delpino, María Victoria Oliveira, Sergio C. Giambartolomei, Guillermo Hernan |
| author2_role |
author author author author author author author author author author author author author |
| dc.subject.none.fl_str_mv |
Hbmec Hbmec Brucella Brucella Neurobrucellosis Neurobrucellosis Inflammasome Inflammasome https://purl.org/becyt/ford/3.1 https://purl.org/becyt/ford/3.1 https://purl.org/becyt/ford/3 https://purl.org/becyt/ford/3 |
| topic |
Hbmec Hbmec Brucella Brucella Neurobrucellosis Neurobrucellosis Inflammasome Inflammasome https://purl.org/becyt/ford/3.1 https://purl.org/becyt/ford/3.1 https://purl.org/becyt/ford/3 https://purl.org/becyt/ford/3 |
| description |
Blood-brain barrier activation and/or dysfunction are a common feature of human neurobrucellosis, but the underlying pathogenic mechanisms are largely unknown. In this article, we describe an immune mechanism for inflammatory activation of human brain microvascular endothelial cells (HBMEC) in response to infection with Brucella abortus Infection of HBMEC with B. abortus induced the secretion of IL-6, IL-8, and MCP-1, and the upregulation of CD54 (ICAM-1), consistent with a state of activation. Culture supernatants (CS) from glial cells (astrocytes and microglia) infected with B. abortus also induced activation of HBMEC, but to a greater extent. Although B. abortus-infected glial cells secreted IL-1β and TNF-α, activation of HBMEC was dependent on IL-1β because CS from B. abortus-infected astrocytes and microglia deficient in caspase-1 and apoptosis-associated speck-like protein containing a CARD failed to induce HBMEC activation. Consistently, treatment of CS with neutralizing anti-IL-1β inhibited HBMEC activation. Both absent in melanoma 2 and Nod-like receptor containing a pyrin domain 3 are partially required for caspase-1 activation and IL-1β secretion, suggesting that multiple apoptosis-associated speck-like protein containing CARD-dependent inflammasomes contribute to IL-1β-induced activation of the brain microvasculature. Inflammasome-mediated IL-1β secretion in glial cells depends on TLR2 and MyD88 adapter-like/TIRAP. Finally, neutrophil and monocyte migration across HBMEC monolayers was increased by CS from Brucella-infected glial cells in an IL-1β-dependent fashion, and the infiltration of neutrophils into the brain parenchyma upon intracranial injection of B. abortus was diminished in the absence of Nod-like receptor containing a pyrin domain 3 and absent in melanoma 2. Our results indicate that innate immunity of the CNS set in motion by B. abortus contributes to the activation of the blood-brain barrier in neurobrucellosis and IL-1β mediates this phenomenon. |
| publishDate |
2016 |
| dc.date.none.fl_str_mv |
2016-03 2016-03 |
| 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/11336/23627 Miraglia, Maria Cruz; Franco, Miriam M. Costa; Rodríguez, Ana María; Bellozi, Paula M. Q.; Ferrari, Carina Cintia; et al.; Glial Cell-Elicited Activation of Brain Microvasculature in Response to Brucella abortus Infection Requires ASC Inflammasome-Dependent IL-1β Production; American Association of Immunologists; Journal of Immunology; 196; 9; 3-2016; 3794-3805 Miraglia, Maria Cruz; Franco, Miriam M. Costa; Rodríguez, Ana María; Bellozi, Paula M. Q.; Ferrari, Carina Cintia; et al.; Glial Cell-Elicited Activation of Brain Microvasculature in Response to Brucella abortus Infection Requires ASC Inflammasome-Dependent IL-1β Production; American Association of Immunologists; Journal of Immunology; 196; 9; 3-2016; 3794-3805 0022-1767 0022-1767 1550-6606 1550-6606 CONICET Digital CONICET |
| url |
http://hdl.handle.net/11336/23627 |
| identifier_str_mv |
Miraglia, Maria Cruz; Franco, Miriam M. Costa; Rodríguez, Ana María; Bellozi, Paula M. Q.; Ferrari, Carina Cintia; et al.; Glial Cell-Elicited Activation of Brain Microvasculature in Response to Brucella abortus Infection Requires ASC Inflammasome-Dependent IL-1β Production; American Association of Immunologists; Journal of Immunology; 196; 9; 3-2016; 3794-3805 0022-1767 1550-6606 CONICET Digital CONICET |
| dc.language.none.fl_str_mv |
eng eng |
| language |
eng |
| dc.relation.none.fl_str_mv |
info:eu-repo/semantics/altIdentifier/url/http://www.jimmunol.org/content/196/9/3794 info:eu-repo/semantics/altIdentifier/url/http://www.jimmunol.org/content/196/9/3794 info:eu-repo/semantics/altIdentifier/doi/10.4049/jimmunol.1500908 info:eu-repo/semantics/altIdentifier/doi/10.4049/jimmunol.1500908 |
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info:eu-repo/semantics/openAccess https://creativecommons.org/licenses/by-nc-sa/2.5/ar/ |
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openAccess |
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application/pdf application/pdf application/pdf application/pdf application/pdf application/pdf application/pdf |
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American Association of Immunologists American Association of Immunologists |
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American Association of Immunologists American Association of Immunologists |
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reponame:CONICET Digital (CONICET) instname:Consejo Nacional de Investigaciones Científicas y Técnicas |
| instname_str |
Consejo Nacional de Investigaciones Científicas y Técnicas |
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CONICET Digital (CONICET) |
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CONICET Digital (CONICET) |
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CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas |
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dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar |
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1799195019392843776 |
| spelling |
Glial Cell-Elicited Activation of Brain Microvasculature in Response to Brucella abortus Infection Requires ASC Inflammasome-Dependent IL-1β ProductionGlial Cell-Elicited Activation of Brain Microvasculature in Response to Brucella abortus Infection Requires ASC Inflammasome-Dependent IL-1β ProductionMiraglia, Maria CruzMiraglia, Maria CruzFranco, Miriam M. CostaFranco, Miriam M. CostaRodríguez, Ana MaríaRodríguez, Ana MaríaBellozi, Paula M. Q.Bellozi, Paula M. Q.Ferrari, Carina CintiaFerrari, Carina CintiaFarias, Maria IsabelFarias, Maria IsabelDennis, Vida A.Dennis, Vida A.Barrionuevo, PaulaBarrionuevo, PaulaOliveira, Antonio C. P. deOliveira, Antonio C. P. dePitossi, Fernando JuanPitossi, Fernando JuanKim, Kwang SikKim, Kwang SikDelpino, María VictoriaDelpino, María VictoriaOliveira, Sergio C.Oliveira, Sergio C.Giambartolomei, Guillermo HernanGiambartolomei, Guillermo HernanHbmecHbmecBrucellaBrucellaNeurobrucellosisNeurobrucellosisInflammasomeInflammasomehttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3https://purl.org/becyt/ford/3Blood-brain barrier activation and/or dysfunction are a common feature of human neurobrucellosis, but the underlying pathogenic mechanisms are largely unknown. In this article, we describe an immune mechanism for inflammatory activation of human brain microvascular endothelial cells (HBMEC) in response to infection with Brucella abortus Infection of HBMEC with B. abortus induced the secretion of IL-6, IL-8, and MCP-1, and the upregulation of CD54 (ICAM-1), consistent with a state of activation. Culture supernatants (CS) from glial cells (astrocytes and microglia) infected with B. abortus also induced activation of HBMEC, but to a greater extent. Although B. abortus-infected glial cells secreted IL-1β and TNF-α, activation of HBMEC was dependent on IL-1β because CS from B. abortus-infected astrocytes and microglia deficient in caspase-1 and apoptosis-associated speck-like protein containing a CARD failed to induce HBMEC activation. Consistently, treatment of CS with neutralizing anti-IL-1β inhibited HBMEC activation. Both absent in melanoma 2 and Nod-like receptor containing a pyrin domain 3 are partially required for caspase-1 activation and IL-1β secretion, suggesting that multiple apoptosis-associated speck-like protein containing CARD-dependent inflammasomes contribute to IL-1β-induced activation of the brain microvasculature. Inflammasome-mediated IL-1β secretion in glial cells depends on TLR2 and MyD88 adapter-like/TIRAP. Finally, neutrophil and monocyte migration across HBMEC monolayers was increased by CS from Brucella-infected glial cells in an IL-1β-dependent fashion, and the infiltration of neutrophils into the brain parenchyma upon intracranial injection of B. abortus was diminished in the absence of Nod-like receptor containing a pyrin domain 3 and absent in melanoma 2. Our results indicate that innate immunity of the CNS set in motion by B. abortus contributes to the activation of the blood-brain barrier in neurobrucellosis and IL-1β mediates this phenomenon.Blood-brain barrier activation and/or dysfunction are a common feature of human neurobrucellosis, but the underlying pathogenic mechanisms are largely unknown. In this article, we describe an immune mechanism for inflammatory activation of human brain microvascular endothelial cells (HBMEC) in response to infection with Brucella abortus Infection of HBMEC with B. abortus induced the secretion of IL-6, IL-8, and MCP-1, and the upregulation of CD54 (ICAM-1), consistent with a state of activation. Culture supernatants (CS) from glial cells (astrocytes and microglia) infected with B. abortus also induced activation of HBMEC, but to a greater extent. Although B. abortus-infected glial cells secreted IL-1β and TNF-α, activation of HBMEC was dependent on IL-1β because CS from B. abortus-infected astrocytes and microglia deficient in caspase-1 and apoptosis-associated speck-like protein containing a CARD failed to induce HBMEC activation. Consistently, treatment of CS with neutralizing anti-IL-1β inhibited HBMEC activation. Both absent in melanoma 2 and Nod-like receptor containing a pyrin domain 3 are partially required for caspase-1 activation and IL-1β secretion, suggesting that multiple apoptosis-associated speck-like protein containing CARD-dependent inflammasomes contribute to IL-1β-induced activation of the brain microvasculature. Inflammasome-mediated IL-1β secretion in glial cells depends on TLR2 and MyD88 adapter-like/TIRAP. Finally, neutrophil and monocyte migration across HBMEC monolayers was increased by CS from Brucella-infected glial cells in an IL-1β-dependent fashion, and the infiltration of neutrophils into the brain parenchyma upon intracranial injection of B. abortus was diminished in the absence of Nod-like receptor containing a pyrin domain 3 and absent in melanoma 2. Our results indicate that innate immunity of the CNS set in motion by B. abortus contributes to the activation of the blood-brain barrier in neurobrucellosis and IL-1β mediates this phenomenon.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; ArgentinaFil: 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; ArgentinaFil: Franco, Miriam M. Costa. Universidade Federal do Minas Gerais; BrasilFil: Franco, Miriam M. Costa. Universidade Federal do Minas Gerais; BrasilFil: Rodríguez, Ana María. 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; ArgentinaFil: Rodríguez, Ana María. 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; ArgentinaFil: Bellozi, Paula M. Q.. Universidade Federal do Minas Gerais; BrasilFil: Bellozi, Paula M. Q.. Universidade Federal do Minas Gerais; BrasilFil: Ferrari, Carina Cintia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; ArgentinaFil: Ferrari, Carina Cintia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; ArgentinaFil: Farias, Maria Isabel. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; ArgentinaFil: Farias, Maria Isabel. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; ArgentinaFil: Dennis, Vida A.. Alabama State University; Estados UnidosFil: Dennis, Vida A.. Alabama State University; Estados UnidosFil: Barrionuevo, Paula. 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; ArgentinaFil: Barrionuevo, Paula. 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; ArgentinaFil: Oliveira, Antonio C. P. de. Universidade Federal do Minas Gerais; BrasilFil: Oliveira, Antonio C. P. de. Universidade Federal do Minas Gerais; BrasilFil: Pitossi, Fernando Juan. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; ArgentinaFil: Pitossi, Fernando Juan. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; ArgentinaFil: Kim, Kwang Sik. University Johns Hopkins; Estados UnidosFil: Kim, Kwang Sik. University Johns Hopkins; Estados UnidosFil: Delpino, María Victoria. 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; ArgentinaFil: Delpino, María Victoria. 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; ArgentinaFil: Oliveira, Sergio C.. Universidade Federal do Minas Gerais; BrasilFil: Oliveira, Sergio C.. Universidade Federal do Minas Gerais; BrasilFil: 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; 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; ArgentinaAmerican Association of ImmunologistsAmerican Association of Immunologists2016-032016-03info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/23627Miraglia, Maria Cruz; Franco, Miriam M. Costa; Rodríguez, Ana María; Bellozi, Paula M. Q.; Ferrari, Carina Cintia; et al.; Glial Cell-Elicited Activation of Brain Microvasculature in Response to Brucella abortus Infection Requires ASC Inflammasome-Dependent IL-1β Production; American Association of Immunologists; Journal of Immunology; 196; 9; 3-2016; 3794-3805Miraglia, Maria Cruz; Franco, Miriam M. Costa; Rodríguez, Ana María; Bellozi, Paula M. Q.; Ferrari, Carina Cintia; et al.; Glial Cell-Elicited Activation of Brain Microvasculature in Response to Brucella abortus Infection Requires ASC Inflammasome-Dependent IL-1β Production; American Association of Immunologists; Journal of Immunology; 196; 9; 3-2016; 3794-38050022-17670022-17671550-66061550-6606CONICET DigitalCONICETengenginfo:eu-repo/semantics/altIdentifier/url/http://www.jimmunol.org/content/196/9/3794info:eu-repo/semantics/altIdentifier/url/http://www.jimmunol.org/content/196/9/3794info:eu-repo/semantics/altIdentifier/doi/10.4049/jimmunol.1500908info:eu-repo/semantics/altIdentifier/doi/10.4049/jimmunol.1500908info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2024-05-08T13:41:29Zoai:ri.conicet.gov.ar:11336/23627instacron: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:34982024-05-08 13:41:29.597CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse |
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15,811543 |