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

dc.creatorBarbosa, Bellisa Freitas de
dc.creatorMaria, Janice Buiate Lopes
dc.creatorGomes, Angelica Oliveira
dc.creatorAngeloni, Mariana Bodini
dc.creatorCastro, Andressa Silva
dc.creatorFranco, Priscila Silva
dc.creatorFermino, Marise Lopes
dc.creatorBarreira, Maria Cristina Roque
dc.creatorIetta, Francesca
dc.creatorMartins Filho, Olindo Assis
dc.creatorSilva, Deise Aparecida Oliveira
dc.creatorMineo, José Roberto
dc.creatorFerro, Eloisa Amália Vieira
dc.date2016-07-01T18:43:55Z
dc.date2016-07-07T11:36:19Z
dc.date2016-07-01T18:43:55Z
dc.date2016-07-07T11:36:19Z
dc.date2015
dc.date.accessioned2023-09-26T20:15:46Z
dc.date.available2023-09-26T20:15:46Z
dc.identifierBARBOSA, Bellisa Freitas de et al. IL10, TGF beta1, and IFN gamma modulate intracellular signaling pathways and cytokine production to control Toxoplasma gondii infection in BeWo trophoblast cells. Biology of Reproduction, v. 92, n. 3, p. 1-13, 2015.
dc.identifier1529-7268
dc.identifierhttps://www.arca.fiocruz.br/handle/icict/14745
dc.identifier10.1095/biolreprod.114.124115
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/8852768
dc.descriptionConsidering 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.
dc.formatapplication/pdf
dc.languageeng
dc.publisherSociety for the Study of Reproduction
dc.rightsopen access
dc.subjectCytokines
dc.subjectSignaling pathways
dc.subjectToxoplasma gondii
dc.subjectTrophoblast cells
dc.titleIL10, TGF beta1, and IFN gamma modulate intracellular signaling pathways and cytokine production to control Toxoplasma gondii infection in BeWo trophoblast cells
dc.typeArticle


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