RESUMEN
Crosstalk between trophoblast and monocytes is essential for gestational success, and it can be compromised in congenital toxoplasmosis. Cell death is one of the mechanisms involved in the maintenance of pregnancy, and this study aimed to evaluate the role of trophoblast in the modulation of monocyte cell death in the presence or absence of Toxoplasma gondii infection. THP-1 cells were stimulated with supernatants of BeWo cells and then infected or not with T. gondii. The supernatants were collected and analyzed for the secretion of human Fas ligand, and cells were used to determine cell death and apoptosis, cell death receptor, and intracellular proteins expression. Cell death and apoptosis index were higher in uninfected THP-1 cells stimulated with supernatants of BeWo cells; however, apoptosis index was reduced by T. gondii infection. Macrophage migration inhibitory factor (MIF) and transforming growth factor (TGF)-ß1, secreted by BeWo cells, altered the cell death and apoptosis rates in THP-1 cells. In infected THP-1 cells, the expression of Fas/CD95 and secretion of FasL was significantly higher; however, caspase 3 and phosphorylated extracellular-signal-regulated kinase (ERK1/2) were downregulated. Results suggest that soluble factors secreted by BeWo cells induce cell death and apoptosis in THP-1 cells, and Fas/CD95 can be involved in this process. On the other hand, T. gondii interferes in the mechanism of cell death and inhibits THP-1 cell apoptosis, which can be associated with active caspase 3 and phosphorylated ERK1/2. In conclusion, our results showed that human BeWo trophoblast cells and T. gondii infection modulate cell death in human THP-1 monocyte cells.
Asunto(s)
Espacio Intracelular/metabolismo , Monocitos/patología , Monocitos/parasitología , Proteínas/metabolismo , Receptores de Muerte Celular/metabolismo , Toxoplasmosis/patología , Trofoblastos/parasitología , Caspasa 3/metabolismo , Muerte Celular/efectos de los fármacos , Línea Celular , Medios de Cultivo Condicionados/farmacología , Regulación hacia Abajo/efectos de los fármacos , Proteína Ligando Fas/metabolismo , Humanos , Sistema de Señalización de MAP Quinasas/efectos de los fármacos , Factores Inhibidores de la Migración de Macrófagos/farmacología , Monocitos/efectos de los fármacos , Monocitos/metabolismo , Fosforilación/efectos de los fármacos , Células THP-1 , Trofoblastos/efectos de los fármacos , Trofoblastos/metabolismo , Receptor fas/metabolismoRESUMEN
Canine hepatozoonosis is a tick-borne disease caused by protozoans of the genus Hepatozoon. Several tick species have been implicated as potential vectors. Therefore, extensive studies are needed to determine the 'natural' endemic cycle of this parasite. This paper presents the first report of the presence of Hepatozoon canis oocysts in Rhipicephalus (Boophilus) microplus collected from an infected dog.