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...

Descripción completa

Guardado en:
Detalles Bibliográficos
Autor principal: Fernández, Andrea Giselle
Otros Autores: Fossati, Carlos A.
Formato: Tesis doctoral acceptedVersion
Lenguaje:Español
Publicado: Facultad de Farmacia y Bioquímica 2019
Materias:
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
Aporte de:
Descripción
Sumario: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.