Autocrine and paracrine IL-6 is necessary to induce phagocytosis of viable neurons by brucella abortus-activated microglia

Autores
Rodríguez, Julia; de Santis Arévalo, Julia; Fiorillo Evequoz, Ariadna Maria; Rodríguez, Ana María; Giambartolomei, Guillermo Hernan
Año de publicación
2022
Idioma
inglés
Tipo de recurso
documento de conferencia
Estado
versión publicada
Descripción
Central nervous system infection by bacteria of the genus Brucella results in an inflammatory disorder called neurobrucellosis. We have previously demonstrated that soluble mediators released by B. abortus-infected astrocytes induce inflammatory activation of microglia and phagocytosis of viable neurons. We have also demonstrated that neutralization of IL-6 in neurons/microglia co-cultures treated with supernatants from B. abortus-infected astrocytes inhibits neuronal death, and this effect is caused by a decrease in the phagocytic activity of microglia. Considering that both astrocytes and microglia are capable of secrete IL-6, we aimed to investigate the contribution of each cell type in this phenomenon. Astrocytes from wild type (WT) and IL-6 KO mice were infected or not with B. abortus for 24 h. After that, cell-free culture supernatants were used to stimulate primary murine co-cultures of WT and IL-6 KO microglia with neurons during 48 h. Neuronal density was evaluated by fluorescence microscopy. Treatment of WT co-cultures with supernatants from IL-6 KO infected astrocytes caused a partial inhibition of neuronal death (p<0.05). Similar results were obtained when neurons/IL-6 KO microglia co-cultures were treated with supernatants from WT- infected astrocytes (p<0.05). Furthermore, neuronal loss was totally prevented in co-cultures of neurons/IL-6 KO microglia treated with IL-6 KO infected astrocytes (p<0.005). Moreover, B. abortus-activated microglia from IL-6 KO mice were unable to induce neuronal death (p<0.05).To evaluate the role of IL-6 in neuronal loss induced by microglia directly activated by B. abortus, we stimulate co-cultures of WT and IL-6 KO microglia with heat-killed B. abortus (HKBA). Activated IL-6 KO microglia were unable to induce neuronal death (p<0.05). These results indicate that both paracrine and autocrine IL-6 signaling in microglia can be sufficient to induce phagocytosis of viable neurons in the context of a B. abortus infection, and could highlight the relevance of this cytokine in neuropathological mechanisms caused by Brucella spp.
Fil: Rodríguez, Julia. 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
Fil: de Santis Arévalo, Julia. 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
Fil: Fiorillo Evequoz, Ariadna Maria. 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
Fil: 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; 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
LXVII Reunión Anual de la Sociedad Argentina de Investigación Clínica; LXX Reunión Anual de la Sociedad Argentina de Inmunología & 3er Congreso Franco Argentino de Inmunología y Reunión Anual 2022 de la Sociedad Argentina de Fisiología
Mar del Plata
Argentina
Sociedad Argentina de Investigación Clínica
Sociedad Argentina de Inmunología
Sociedad Argentina de Fisiología
Materia
microglia
IL-6
Neuronas
B. abortus
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:11336/242597
Acceder
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network_name_str CONICET Digital (CONICET)
spelling Autocrine and paracrine IL-6 is necessary to induce phagocytosis of viable neurons by brucella abortus-activated microgliaRodríguez, Juliade Santis Arévalo, JuliaFiorillo Evequoz, Ariadna MariaRodríguez, Ana MaríaGiambartolomei, Guillermo HernanmicrogliaIL-6NeuronasB. abortushttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Central nervous system infection by bacteria of the genus Brucella results in an inflammatory disorder called neurobrucellosis. We have previously demonstrated that soluble mediators released by B. abortus-infected astrocytes induce inflammatory activation of microglia and phagocytosis of viable neurons. We have also demonstrated that neutralization of IL-6 in neurons/microglia co-cultures treated with supernatants from B. abortus-infected astrocytes inhibits neuronal death, and this effect is caused by a decrease in the phagocytic activity of microglia. Considering that both astrocytes and microglia are capable of secrete IL-6, we aimed to investigate the contribution of each cell type in this phenomenon. Astrocytes from wild type (WT) and IL-6 KO mice were infected or not with B. abortus for 24 h. After that, cell-free culture supernatants were used to stimulate primary murine co-cultures of WT and IL-6 KO microglia with neurons during 48 h. Neuronal density was evaluated by fluorescence microscopy. Treatment of WT co-cultures with supernatants from IL-6 KO infected astrocytes caused a partial inhibition of neuronal death (p<0.05). Similar results were obtained when neurons/IL-6 KO microglia co-cultures were treated with supernatants from WT- infected astrocytes (p<0.05). Furthermore, neuronal loss was totally prevented in co-cultures of neurons/IL-6 KO microglia treated with IL-6 KO infected astrocytes (p<0.005). Moreover, B. abortus-activated microglia from IL-6 KO mice were unable to induce neuronal death (p<0.05).To evaluate the role of IL-6 in neuronal loss induced by microglia directly activated by B. abortus, we stimulate co-cultures of WT and IL-6 KO microglia with heat-killed B. abortus (HKBA). Activated IL-6 KO microglia were unable to induce neuronal death (p<0.05). These results indicate that both paracrine and autocrine IL-6 signaling in microglia can be sufficient to induce phagocytosis of viable neurons in the context of a B. abortus infection, and could highlight the relevance of this cytokine in neuropathological mechanisms caused by Brucella spp.Fil: Rodríguez, Julia. 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: de Santis Arévalo, Julia. 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: Fiorillo Evequoz, Ariadna Maria. 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: 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; ArgentinaLXVII Reunión Anual de la Sociedad Argentina de Investigación Clínica; LXX Reunión Anual de la Sociedad Argentina de Inmunología & 3er Congreso Franco Argentino de Inmunología y Reunión Anual 2022 de la Sociedad Argentina de FisiologíaMar del PlataArgentinaSociedad Argentina de Investigación ClínicaSociedad Argentina de InmunologíaSociedad Argentina de FisiologíaFundación Revista Medicina2022info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/conferenceObjectReuniónJournalhttp://purl.org/coar/resource_type/c_5794info:ar-repo/semantics/documentoDeConferenciaapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/242597Autocrine and paracrine IL-6 is necessary to induce phagocytosis of viable neurons by brucella abortus-activated microglia; LXVII Reunión Anual de la Sociedad Argentina de Investigación Clínica; LXX Reunión Anual de la Sociedad Argentina de Inmunología & 3er Congreso Franco Argentino de Inmunología y Reunión Anual 2022 de la Sociedad Argentina de Fisiología; Mar del Plata; Argentina; 2022; 1-20025-76801669-9106CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://medicinabuenosaires.com/revistas/vol82-22/s5/1s5.pdfInternacionalinfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T09:45:47Zoai:ri.conicet.gov.ar:11336/242597instacron: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 09:45:48.184CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Autocrine and paracrine IL-6 is necessary to induce phagocytosis of viable neurons by brucella abortus-activated microglia
title Autocrine and paracrine IL-6 is necessary to induce phagocytosis of viable neurons by brucella abortus-activated microglia
spellingShingle Autocrine and paracrine IL-6 is necessary to induce phagocytosis of viable neurons by brucella abortus-activated microglia
Rodríguez, Julia
microglia
IL-6
Neuronas
B. abortus
title_short Autocrine and paracrine IL-6 is necessary to induce phagocytosis of viable neurons by brucella abortus-activated microglia
title_full Autocrine and paracrine IL-6 is necessary to induce phagocytosis of viable neurons by brucella abortus-activated microglia
title_fullStr Autocrine and paracrine IL-6 is necessary to induce phagocytosis of viable neurons by brucella abortus-activated microglia
title_full_unstemmed Autocrine and paracrine IL-6 is necessary to induce phagocytosis of viable neurons by brucella abortus-activated microglia
title_sort Autocrine and paracrine IL-6 is necessary to induce phagocytosis of viable neurons by brucella abortus-activated microglia
dc.creator.none.fl_str_mv Rodríguez, Julia
de Santis Arévalo, Julia
Fiorillo Evequoz, Ariadna Maria
Rodríguez, Ana María
Giambartolomei, Guillermo Hernan
author Rodríguez, Julia
author_facet Rodríguez, Julia
de Santis Arévalo, Julia
Fiorillo Evequoz, Ariadna Maria
Rodríguez, Ana María
Giambartolomei, Guillermo Hernan
author_role author
author2 de Santis Arévalo, Julia
Fiorillo Evequoz, Ariadna Maria
Rodríguez, Ana María
Giambartolomei, Guillermo Hernan
author2_role author
author
author
author
dc.subject.none.fl_str_mv microglia
IL-6
Neuronas
B. abortus
topic microglia
IL-6
Neuronas
B. abortus
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Central nervous system infection by bacteria of the genus Brucella results in an inflammatory disorder called neurobrucellosis. We have previously demonstrated that soluble mediators released by B. abortus-infected astrocytes induce inflammatory activation of microglia and phagocytosis of viable neurons. We have also demonstrated that neutralization of IL-6 in neurons/microglia co-cultures treated with supernatants from B. abortus-infected astrocytes inhibits neuronal death, and this effect is caused by a decrease in the phagocytic activity of microglia. Considering that both astrocytes and microglia are capable of secrete IL-6, we aimed to investigate the contribution of each cell type in this phenomenon. Astrocytes from wild type (WT) and IL-6 KO mice were infected or not with B. abortus for 24 h. After that, cell-free culture supernatants were used to stimulate primary murine co-cultures of WT and IL-6 KO microglia with neurons during 48 h. Neuronal density was evaluated by fluorescence microscopy. Treatment of WT co-cultures with supernatants from IL-6 KO infected astrocytes caused a partial inhibition of neuronal death (p<0.05). Similar results were obtained when neurons/IL-6 KO microglia co-cultures were treated with supernatants from WT- infected astrocytes (p<0.05). Furthermore, neuronal loss was totally prevented in co-cultures of neurons/IL-6 KO microglia treated with IL-6 KO infected astrocytes (p<0.005). Moreover, B. abortus-activated microglia from IL-6 KO mice were unable to induce neuronal death (p<0.05).To evaluate the role of IL-6 in neuronal loss induced by microglia directly activated by B. abortus, we stimulate co-cultures of WT and IL-6 KO microglia with heat-killed B. abortus (HKBA). Activated IL-6 KO microglia were unable to induce neuronal death (p<0.05). These results indicate that both paracrine and autocrine IL-6 signaling in microglia can be sufficient to induce phagocytosis of viable neurons in the context of a B. abortus infection, and could highlight the relevance of this cytokine in neuropathological mechanisms caused by Brucella spp.
Fil: Rodríguez, Julia. 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
Fil: de Santis Arévalo, Julia. 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
Fil: Fiorillo Evequoz, Ariadna Maria. 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
Fil: 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; 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
LXVII Reunión Anual de la Sociedad Argentina de Investigación Clínica; LXX Reunión Anual de la Sociedad Argentina de Inmunología & 3er Congreso Franco Argentino de Inmunología y Reunión Anual 2022 de la Sociedad Argentina de Fisiología
Mar del Plata
Argentina
Sociedad Argentina de Investigación Clínica
Sociedad Argentina de Inmunología
Sociedad Argentina de Fisiología
description Central nervous system infection by bacteria of the genus Brucella results in an inflammatory disorder called neurobrucellosis. We have previously demonstrated that soluble mediators released by B. abortus-infected astrocytes induce inflammatory activation of microglia and phagocytosis of viable neurons. We have also demonstrated that neutralization of IL-6 in neurons/microglia co-cultures treated with supernatants from B. abortus-infected astrocytes inhibits neuronal death, and this effect is caused by a decrease in the phagocytic activity of microglia. Considering that both astrocytes and microglia are capable of secrete IL-6, we aimed to investigate the contribution of each cell type in this phenomenon. Astrocytes from wild type (WT) and IL-6 KO mice were infected or not with B. abortus for 24 h. After that, cell-free culture supernatants were used to stimulate primary murine co-cultures of WT and IL-6 KO microglia with neurons during 48 h. Neuronal density was evaluated by fluorescence microscopy. Treatment of WT co-cultures with supernatants from IL-6 KO infected astrocytes caused a partial inhibition of neuronal death (p<0.05). Similar results were obtained when neurons/IL-6 KO microglia co-cultures were treated with supernatants from WT- infected astrocytes (p<0.05). Furthermore, neuronal loss was totally prevented in co-cultures of neurons/IL-6 KO microglia treated with IL-6 KO infected astrocytes (p<0.005). Moreover, B. abortus-activated microglia from IL-6 KO mice were unable to induce neuronal death (p<0.05).To evaluate the role of IL-6 in neuronal loss induced by microglia directly activated by B. abortus, we stimulate co-cultures of WT and IL-6 KO microglia with heat-killed B. abortus (HKBA). Activated IL-6 KO microglia were unable to induce neuronal death (p<0.05). These results indicate that both paracrine and autocrine IL-6 signaling in microglia can be sufficient to induce phagocytosis of viable neurons in the context of a B. abortus infection, and could highlight the relevance of this cytokine in neuropathological mechanisms caused by Brucella spp.
publishDate 2022
dc.date.none.fl_str_mv 2022
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dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/242597
Autocrine and paracrine IL-6 is necessary to induce phagocytosis of viable neurons by brucella abortus-activated microglia; LXVII Reunión Anual de la Sociedad Argentina de Investigación Clínica; LXX Reunión Anual de la Sociedad Argentina de Inmunología & 3er Congreso Franco Argentino de Inmunología y Reunión Anual 2022 de la Sociedad Argentina de Fisiología; Mar del Plata; Argentina; 2022; 1-2
0025-7680
1669-9106
CONICET Digital
CONICET
url http://hdl.handle.net/11336/242597
identifier_str_mv Autocrine and paracrine IL-6 is necessary to induce phagocytosis of viable neurons by brucella abortus-activated microglia; LXVII Reunión Anual de la Sociedad Argentina de Investigación Clínica; LXX Reunión Anual de la Sociedad Argentina de Inmunología & 3er Congreso Franco Argentino de Inmunología y Reunión Anual 2022 de la Sociedad Argentina de Fisiología; Mar del Plata; Argentina; 2022; 1-2
0025-7680
1669-9106
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
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publisher.none.fl_str_mv Fundación Revista Medicina
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