Transforming growth factor (TGF)-β1 and interferon (IFN)-γ differentially regulate ICAM-1 expression and adhesion of Toxoplasma gondii to human trophoblast (BeWo) and uterine cervical (HeLa) cells

Toxoplasma gondii is a parasite able to infect various cell types, including trophoblast cells. Studies have demonstrated that interleukin (IL)-10, transforming growth factor (TGF)-β1 and interferon (IFN)-γ are involved in the susceptibility of BeWo trophoblast cells to T. gondii infection. Furtherm...

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Published in:Acta tropica 2021-12, Vol.224, p.106111-106111, Article 106111
Main Authors: Teixeira, Samuel Cota, Silva, Rafaela J., Lopes-Maria, Janice B., Gomes, Angelica O., Angeloni, Mariana B., Fermino, Marise L., Roque-Barreira, Maria C., Silva, Neide M., Silva, Deise A.O., Mineo, José R., Ferro, Eloisa A.V., Barbosa, Bellisa F.
Format: Article
Language:English
Subjects:
BeWo trophoblast cells
HeLa cells
ICAM-1
IFN-γ
TGF-β1
Toxoplasma gondii
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Summary:Toxoplasma gondii is a parasite able to infect various cell types, including trophoblast cells. Studies have demonstrated that interleukin (IL)-10, transforming growth factor (TGF)-β1 and interferon (IFN)-γ are involved in the susceptibility of BeWo trophoblast cells to T. gondii infection. Furthermore, T. gondii is able to adhere to the plasma membrane of host cells through intercellular adhesion molecule (ICAM)-1. Thus, the present study aimed to assess the role of IL-10, TGF-β1 and IFN-γ in the expression of ICAM-1 in BeWo and HeLa cells and to analyze the role of ICAM-1 in the adhesion and invasion of T. gondii to these cells under the influence of these cytokines. For this purpose, BeWo and HeLa cells were treated or not, before and after T. gondii infection, with rIL-10, rTGF-β1 or rIFN-γ. For the BeWo cells, rIL-10 and rTGF-β1 favored susceptibility to infection, but only rTGF-β1 and rIFN-γ increased ICAM-1 expression, and TNF-α release. On the other hand, rIFN-γ downregulated the expression of ICAM-1 triggered by T. gondii in HeLa cells, leading to control of the infection. Moreover, we observed that upregulation of ICAM-1, mediated by cytokine's stimulation, in BeWo and HeLa cells resulted in a high number rate of both parasite adhesion and invasion to these cells, which were strongly reduced after ICAM-1 neutralization. Likewise, the blockage of ICAM-1 molecule also impaired T. gondii infection in human villous explants. Taken together, these findings demonstrate that TGF-β1 and IFN-γ differentially regulate ICAM-1 expression, which may interfere in the adhesion/invasion of T. gondii to BeWo and HeLa cells for modulating susceptibility to infection. •TGF-β1 increases the susceptibility of BeWo trophoblast cells to T. gondii.•TGF-β1 and IFN-γ upregulate ICAM-1 in BeWo trophoblast cells infected by T. gondii.•TGF-β1 and IFN-γ decrease ICAM-1 in HeLa cells infected by T. gondii.•High levels of TNF-α are associated with increased expression of ICAM-1.•Increased ICAM-1 expression trigger high number of membrane-adhered T. gondii. Proposed model summarizes the influence of the cytokines TGF-β1 and IFN-γ on the expression of ICAM-1 in BeWo and HeLa cells infected by T. gondii. [Display omitted]
ISSN:0001-706X
1873-6254
DOI:10.1016/j.actatropica.2021.106111