特里夫
生物
弓形虫
TLR4型
分子生物学
下调和上调
细胞因子
细胞生物学
Toll样受体
免疫学
信号转导
免疫系统
先天免疫系统
生物化学
抗体
基因
作者
Alessandra Monteiro Rosini,Samuel Cota Teixeira,Iliana Claudia Balga Milián,Rafaela A. L. Silva,Guilherme Silva Freire de Souza,Luana Carvalho Luz,A.O. Gomes,José Roberto Mineo,José Roberto Mineo,Eloisa Amália Vieira Ferro,B.F. Barbosa
出处
期刊:Tissue & Cell
[Elsevier]
日期:2022-10-01
卷期号:78: 101907-101907
被引量:1
标识
DOI:10.1016/j.tice.2022.101907
摘要
We evaluated the influence of the Toll-like receptor (TLR)-4 pathways on BeWo, JEG-3 and HTR-8/SVneo cells, as well as in human villous explants infected with Toxoplasma gondii. Cells and explants were stimulated with LPS for 24 or 48 h and processed for the MTT assay, and expression of TLR4 was evaluated by confocal microscopy. In addition, we used peptides that inhibit MyD88 or TRIF, and inhibitor to NF-κB. Finally, the parasite proliferation was verified, and ELISA was performed to verify the cytokine production. As results, LPS did not induce toxicity in cells and explants. However, LPS triggered a reduction in T. gondii proliferation only in BeWo cells and explants. Additionally, LPS downmodulated IL-10, TGF-β1 and TNF, but upregulated IFN-γ in BeWo cells. For explants, LPS induced high levels of IL-10, TGF-β1 and IFN-γ. Finally, it was observed that the inhibition of TRIF and NF-κB increased parasitism and modulated TGF-β1 in BeWo cells, while the inhibition of MyD88 and NF-κB increased T. gondii infection and modulated IFN-γ in explants. It can be concluded that the TLR4 pathway is important for the control of T. gondii replication in BeWo cells and villous explants, in a dependent-manner of TRIF, MyD88, NF-κB and cytokines.
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