IL10, TGF beta1, and IFN gamma modulate intracellular signaling pathways and cytokine production to control Toxoplasma gondii infection in BeWo trophoblast cells

Considering that interleukin 10 (IL10), transforming growth factor beta1 (TGFB1), and interferon gamma (IFNG) are involved in the susceptibility of BeWo trophoblast cells to Toxoplasma gondii infection, the aim of the present study was to investigate the effector mechanisms triggered by these cytoki...

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Bibliographic Details
Published in:Biology of reproduction 2015-03, Vol.92 (3), p.82-82
Main Authors: Barbosa, Bellisa Freitas, Lopes-Maria, Janice Buiate, Gomes, Angelica Oliveira, Angeloni, Mariana Bodini, Castro, Andressa Silva, Franco, Priscila Silva, Fermino, Marise Lopes, Roque-Barreira, Maria Cristina, Ietta, Francesca, Martins-Filho, Olindo Assis, Silva, Deise Aparecida Oliveira, Mineo, José Roberto, Ferro, Eloisa Amália Vieira
Format: Article
Language:English
Subjects:
Cell Line, Tumor
Choriocarcinoma - pathology
Cytokines - metabolism
Disease Susceptibility
Female
Humans
In Vitro Techniques
Interferon-gamma - pharmacology
Interleukin-10 - pharmacology
Interleukin-16 - metabolism
Phosphorylation
Pregnancy
Signal Transduction - drug effects
Signal Transduction - physiology
Smad2 Protein - metabolism
STAT1 Transcription Factor - metabolism
STAT3 Transcription Factor - metabolism
Toxoplasma - isolation & purification
Toxoplasmosis - metabolism
Toxoplasmosis - pathology
Toxoplasmosis - prevention & control
Transforming Growth Factor beta1 - pharmacology
Trophoblasts - drug effects
Trophoblasts - metabolism
Trophoblasts - parasitology
Tumor Necrosis Factor-alpha - metabolism
Uterine Neoplasms - pathology
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Summary:Considering that interleukin 10 (IL10), transforming growth factor beta1 (TGFB1), and interferon gamma (IFNG) are involved in the susceptibility of BeWo trophoblast cells to Toxoplasma gondii infection, the aim of the present study was to investigate the effector mechanisms triggered by these cytokines in the control of T. gondii in BeWo cells. For this purpose, infected/uninfected BeWo cells were treated with IL10, TGFB1 (50 ng/ml), and IFNG (20 or 100 ng/ml) in order to verify the phosphorylation of signal transducers and activators of transcription 1 (STAT1), STAT3, and Smad2, parasite intracellular proliferation, as well as the Th1/Th2/IL17A cytokine production. The treatment of BeWo cells with IL10 and TGFB1 favored T. gondii proliferation, and these findings were associated with STAT3 and Smad2 phosphorylation, respectively (P < 0.05). Also, these cytokine treatments were able to down-modulate TNF alpha (TNFA) and IL6 production (P < 0.05). Low concentration of IFNG was unable to control T. gondii infection but was able to trigger STAT1 phosphorylation and up-regulate IL6 and IL17A production; whereas a high concentration of IFNG was unable to activate STAT1 but down-modulated IL6 and TNFA and increased T. gondii proliferation (P < 0.05). IL10, TGFB1, and IFNG regulate a differential T. gondii proliferation in BeWo cells because they distinctly trigger intracellular signaling pathways and cytokine production, especially IL6 and TNFA. Our data open new windows to understand the mechanisms triggered by IL10, TGFB1, and IFNG at the maternal-fetal interface in the presence of T. gondii, contributing to recognizing the importance of these effector mechanisms involved in the vertical transmission of this parasite.
ISSN:1529-7268
DOI:10.1095/biolreprod.114.124115