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首页> 外文期刊>Archives of Toxicology >Isoeugenol destabilizes IL-8 mRNA expression in THP-1 cells through induction of the negative regulator of mRNA stability tristetraprolin
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Isoeugenol destabilizes IL-8 mRNA expression in THP-1 cells through induction of the negative regulator of mRNA stability tristetraprolin

机译：异丁香酚通过诱导mRNA稳定性tristetraprolin负调节剂破坏THP-1细胞中IL-8 mRNA的表达

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摘要

We previously demonstrated in the human promyelocytic cell line THP-1 that all allergens tested, with the exception of the prohapten isoeugenol, induced a dose-related release of interleukin-8 (IL-8). In the present study, we investigated whether this abnormal behavior was regulated by the AU-rich element-binding proteins HuR and tristetraprolin (TTP) or by the downstream molecule suppressor of cytokine signaling (SOCS)-3. The contact allergens isoeugenol, diethylmaleate (DEM), and 2,4-dinitrochlorobenzene (DNCB), and the irritant salicylic acid were used as reference compounds. Chemicals were used at concentrations that induced a 20% decrease in cell viability as assessed by propidium iodide staining, namely 100 μg/ml (0.61 mM) for isoeugenol, 100 μg/ml (0.58 mM) for DEM, 3 μg/ml (14.8 μM) for DNCB, and 250 μg/ml (1.81 mM) for salicylic acid. Time course experiments of IL-8 mRNA expression and assessment of IL-8 mRNA half-life, indicated a decreased IL-8 mRNA stability in isoeugenol-treated cells. We could demonstrate that a combination and regulation of HuR and TTP following exposure to contact allergens resulted in a different modulation of IL-8 mRNA half-life and release. The increased expression of TTP in THP-1 cells treated with isoeugenol results in destabilization of the IL-8 mRNA, which can account for the lack of IL-8 release. In contrast, the strong allergen DNCB failing to up-regulate TTP, while inducing HuR, resulted in longer IL-8 mRNA half-life and protein release. SOCS-3 was induced only in isoeugenol-treated cells; however, its modulation did not rescue the lack of IL-8 release, indicating that it is unlikely to be involved in the lack of IL-8 production. Finally, the destabilization effect of isoeugenol on IL-8 mRNA expression together with SOCS-3 expression resulted in an anti-inflammatory effect, as demonstrated by the ability of isoeugenol to modulate LPS or ionomycin-induced cytokine release.
机译：我们先前在人类早幼粒细胞细胞THP-1中证明，除半抗原异丁香酚外，所有测试的过敏原均诱导了白介素8（IL-8）的剂量相关释放。在本研究中，我们调查了这种异常行为是否受富含AU的元素结合蛋白HuR和tristetraprolin（TTP）或细胞因子信号传导的下游分子抑制剂（SOCS）-3调控。接触过敏原异丁香酚，马来酸二乙酯（DEM）和2,4-二硝基氯苯（DNCB）以及刺激性水杨酸用作参考化合物。通过碘化丙锭染色评估，化学药品的使用浓度可导致细胞活力降低20％，即异丁香酚为100μg/ ml（0.61 mM），DEM为100μg/ ml（0.58 mM），3μg/ ml（14.8） DNCB为250μg/ ml（1.81 mM）。 IL-8 mRNA表达的时程实验和IL-8 mRNA半衰期的评估表明，在异丁香酚处理的细胞中IL-8 mRNA的稳定性降低。我们可以证明，接触接触变应原后，HuR和TTP的组合和调节导致IL-8 mRNA半衰期和释放的不同调节。 TTP在异丁香酚处理过的THP-1细胞中表达的增加导致IL-8 mRNA的不稳定，这可以解释IL-8释放的缺乏。相比之下，强变应原DNCB在诱导HuR时未能上调TTP，导致更长的IL-8 mRNA半衰期和蛋白质释放。 SOCS-3仅在异丁香酚处理的细胞中诱导;但是，其调节不能挽救缺乏IL-8的释放，这表明它不太可能与缺乏IL-8的产生有关。最后，异丁香酚对IL-8 mRNA表达的去稳定作用与SOCS-3表达一起导致了抗炎作用，如异丁香酚调节LPS或离子霉素诱导的细胞因子释放的能力所证实。

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