Interacción de Brucella spp. con células de la interfase materno-fetal

Brucella spp. infection triggers abortion in different hosts and, although the pathophysiological mechanisms involved in fetal death are still unknown, trophoblasts are known to be targets of the infection and to be surrounded by an inflammatory infiltrate. To characterize the placental immune respo...

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Autor principal: Fernández, Andrea Giselle
Otros Autores: Fossati, Carlos A.
Formato: Tesis doctoral acceptedVersion
Lenguaje:Español
Publicado: Facultad de Farmacia y Bioquímica 2019
Materias:
Brucella
Trofoblastos
Aborto
Fagositos
Ciencias de la vida
Acceso en línea:http://repositoriouba.sisbi.uba.ar/gsdl/cgi-bin/library.cgi?a=d&c=posgraafa&cl=CL1&d=HWA_2828
http://repositoriouba.sisbi.uba.ar/gsdl/collect/posgraafa/index/assoc/HWA_2828.dir/2828.PDF
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Repositorio Digital de la Universidad de Buenos Aires (UBA) de Universidad de Buenos Aires
id I28-R145-HWA_2828
record_format dspace
spelling I28-R145-HWA_28282020-07-05 Brucella spp. infection triggers abortion in different hosts and, although the pathophysiological mechanisms involved in fetal death are still unknown, trophoblasts are known to be targets of the infection and to be surrounded by an inflammatory infiltrate. To characterize the placental immune response, and to evaluate the role of trophoblasts, macrophages, neutrophils and endometrial cells during infection, human and canine cells were infected with B. abortus and B. canis, respectively. Thus, we demonstrated that Brucella spp. is able to replicate in trophoblastic cells, eliciting a proinflammatory response mediated by IL-8/CXCL8, IL-6, MCP-1/CCL2 and/or RANTES/CCL5, which is increased trough IL-1? and TNF-? secreted by infected phagocytes. The increase in chemokines favors the inflammatory infiltrate, and the interaction between placental cells and phagocytes, all of them susceptible to Brucella spp. infection, stimulates the increase in proinflammatory cytokines and metalloproteinases (MMP-2 and MMP-9) with the ability to induce placental damage trough trophoblast apoptosis and weakening of fetal membranes. Globally, these mechanisms could provoke the loss of maternal-fetal interface tolerance and the triggering of abortion in Brucella-infected pregnant hosts. Fil: Fernández, Andrea Giselle. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Buenos Aires, Argentina Fossati, Carlos A. Facultad de Farmacia y Bioquímica Baldi, Pablo C. Fernández, Andrea Giselle 2019-04-04 Brucella spp. produce aborto en diferentes huéspedes, y aunque los mecanismos fisiopatológicos involucrados se desconocen, es sabido que los trofoblastos son blanco de la infección con esta bacteria y que se rodean de infiltrado inflamatorio. Con el objetivo de caracterizar la respuesta inmune placentaria y evaluar el rol que cumplen trofoblastos, macrófagos, neutrófilos y células endometriales durante la infección, se infectaron células humanas y caninas con B. abortus y B. canis, respectivamente. Así, demostramos que Brucella spp. es capaz de replicar en células trofoblásticas generando una respuesta proinflamatoria mediada por IL-8/CXCL8, IL-6, MCP-1/CCL2 y/o RANTES/CCL5, la cual es potenciada por IL-1? y TNF-? secretados por fagocitos infectados. El aumento de quimioquinas favorecería el infiltrado inflamatorio, y la interacción entre las células placentarias y los fagocitos, todos ellos susceptibles a la infección con Brucella spp., potencia el aumento de citoquinas proinflamatorias y metaloproteinasas (MMP-2 y MMP-9) con la capacidad de generar daño placentario mediante apoptosis del trofoblasto y debilitamiento de las membranas fetales. Globalmente, estos mecanismos podrían provocar la pérdida de la tolerancia en la interfase materno-fetal y el desencadenamiento del aborto en huéspedes preñados infectados con Brucella spp. application/pdf Canellada, Andrea Franchi, Ana Samartino, Luis Brucella Trofoblastos Aborto Fagositos spa Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by-nc-nd/2.5/ar/ Ciencias de la vida Interacción de Brucella spp. con células de la interfase materno-fetal info:eu-repo/semantics/doctoralThesis info:ar-repo/semantics/tesis doctoral info:eu-repo/semantics/acceptedVersion http://repositoriouba.sisbi.uba.ar/gsdl/cgi-bin/library.cgi?a=d&c=posgraafa&cl=CL1&d=HWA_2828 http://repositoriouba.sisbi.uba.ar/gsdl/collect/posgraafa/index/assoc/HWA_2828.dir/2828.PDF
institution Universidad de Buenos Aires
institution_str I-28
repository_str R-145
collection Repositorio Digital de la Universidad de Buenos Aires (UBA)
language Español
orig_language_str_mv spa
topic Brucella
Trofoblastos
Aborto
Fagositos
Ciencias de la vida
spellingShingle Brucella
Trofoblastos
Aborto
Fagositos
Ciencias de la vida
Fernández, Andrea Giselle
Interacción de Brucella spp. con células de la interfase materno-fetal
topic_facet Brucella
Trofoblastos
Aborto
Fagositos
Ciencias de la vida
description Brucella spp. infection triggers abortion in different hosts and, although the pathophysiological mechanisms involved in fetal death are still unknown, trophoblasts are known to be targets of the infection and to be surrounded by an inflammatory infiltrate. To characterize the placental immune response, and to evaluate the role of trophoblasts, macrophages, neutrophils and endometrial cells during infection, human and canine cells were infected with B. abortus and B. canis, respectively. Thus, we demonstrated that Brucella spp. is able to replicate in trophoblastic cells, eliciting a proinflammatory response mediated by IL-8/CXCL8, IL-6, MCP-1/CCL2 and/or RANTES/CCL5, which is increased trough IL-1? and TNF-? secreted by infected phagocytes. The increase in chemokines favors the inflammatory infiltrate, and the interaction between placental cells and phagocytes, all of them susceptible to Brucella spp. infection, stimulates the increase in proinflammatory cytokines and metalloproteinases (MMP-2 and MMP-9) with the ability to induce placental damage trough trophoblast apoptosis and weakening of fetal membranes. Globally, these mechanisms could provoke the loss of maternal-fetal interface tolerance and the triggering of abortion in Brucella-infected pregnant hosts.
author2 Fossati, Carlos A.
author_facet Fossati, Carlos A.
Fernández, Andrea Giselle
format Tesis doctoral
Tesis doctoral
acceptedVersion
author Fernández, Andrea Giselle
author_sort Fernández, Andrea Giselle
title Interacción de Brucella spp. con células de la interfase materno-fetal
title_short Interacción de Brucella spp. con células de la interfase materno-fetal
title_full Interacción de Brucella spp. con células de la interfase materno-fetal
title_fullStr Interacción de Brucella spp. con células de la interfase materno-fetal
title_full_unstemmed Interacción de Brucella spp. con células de la interfase materno-fetal
title_sort interacción de brucella spp. con células de la interfase materno-fetal
publisher Facultad de Farmacia y Bioquímica
publishDate 2019
url http://repositoriouba.sisbi.uba.ar/gsdl/cgi-bin/library.cgi?a=d&c=posgraafa&cl=CL1&d=HWA_2828
http://repositoriouba.sisbi.uba.ar/gsdl/collect/posgraafa/index/assoc/HWA_2828.dir/2828.PDF
work_keys_str_mv AT fernandezandreagiselle interacciondebrucellasppconcelulasdelainterfasematernofetal
_version_ 1766017518576599040

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