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聚肌苷酸胞苷酸(Poly I:C)和呼吸道合胞病毒(RSV)抑制肺上皮细胞而不是单核细胞系中糖皮质激素受体(GR)介导的转激活作用。

Poly I:C and respiratory syncytial virus (RSV) inhibit glucocorticoid receptor (GR)-mediated transactivation in lung epithelial, but not monocytic, cell lines.

机构信息

Division of Pulmonary, Allergy, Critical Care and Sleep Medicine, Department of Internal Medicine, Wexner Medical Center at The Ohio State University, Columbus, OH 43210, United States.

出版信息

Virus Res. 2013 Sep;176(1-2):303-6. doi: 10.1016/j.virusres.2013.06.011. Epub 2013 Jul 2.

Abstract

Respiratory syncytial virus (RSV)-induced bronchiolitis in infants is not responsive to glucocorticoids. We have recently shown that RSV infection of lung epithelial cells impairs glucocorticoid receptor (GR) function. In this current study, we have shown that the viral mimic poly I:C also represses GR-mediated gene activation in lung epithelial cells, suggesting that this might be a common phenomenon of other viral infections. However, we also show that neither RSV infection nor poly I:C affect GR-mediated gene activation in the monocytic cell line THP-1, suggesting that these effects on GR function may be cell-type specific.

摘要

婴儿呼吸道合胞病毒(RSV)引起的细支气管炎对糖皮质激素无反应。我们最近表明,RSV 感染肺上皮细胞会损害糖皮质激素受体(GR)的功能。在本研究中,我们表明病毒类似物聚肌胞苷酸(poly I:C)也会抑制肺上皮细胞中 GR 介导的基因激活,表明这可能是其他病毒感染的共同现象。然而,我们还表明,RSV 感染或 poly I:C 既不影响单核细胞系 THP-1 中的 GR 介导的基因激活,这表明这些对 GR 功能的影响可能是细胞类型特异性的。

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