| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 2788475 | Placenta | 2015 | 9 Pages |
•Toxoplasma. gondii infection modulates cytokine production in macrophages.•Cytokine secretion in HTR-8 cells is modulated by macrophages and T. gondii infection.•Apoptosis in HTR-8 cells is modulated by macrophages and T. gondii infection.•Mediators triggered by macrophages and infection modulate the apoptosis in HTR-8 cells.•T. gondii infection is able to modulate the trophoblast-macrophage crosstalk.
IntroductionThe interaction between human extravillous trophoblasts and macrophages has an important role in implantation and placentation. However, any dysfunction in this communication system is associated with pregnancy pitfalls, and a Toxoplasma gondii infection can be a potential problem in this crosstalk. Therefore, the aim of this study was to assess the influence of infected macrophages on cytokine production and the incidence of apoptosis in T. gondii-infected extravillous trophoblast cells.MethodsHTR-8/SVneo cells were treated with supernatant from macrophages infected or not by T. gondii (conditioned medium) in order to analyze apoptosis and cytokine production in comparison to uninfected control conditions.ResultsThe IL-6 secretion by HTR-8/SVneo cells increased synergistically by treatment with conditioned medium and T. gondii infection. The apoptosis index of HTR-8/SVneo cells was also upregulated by treatment with conditioned medium and infection. In addition, a low expression of Fas/CD95 and a high soluble FasL release were observed during infection, although no significant change was observed in the proliferation of T. gondii.DiscussionThe parasite modulates the high apoptosis index in HTR-8/SVneo cells in order to favor its establishment inside its host cells. On the other hand, the conditioned medium from uninfected macrophages restores the apoptosis rates, although the effect of the infection seems to be stronger. In conclusion, our results showed that T. gondii infection in human extravillous trophoblasts is able to modulate the trophoblast-macrophage crosstalk.
