IL-1β-induced ICAM-1 and IL-8 expression/secretion of dental pulp cells is differentially regulated by IRAK and p38
IL-1β-induced ICAM-1 and IL-8 expression/secretion of dental pulp cells is differentially regulated by IRAK and p38
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DOI：
10.1016/j.jfma.2018.11.015
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发表时间：
2019-08-01
影响因子：
3.2
通讯作者：
Jeng, Jiiang-Huei
中科院分区：
文献类型：
--
作者：
Chang, Mei-Chi;Lin, Szu-, I;Jeng, Jiiang-Huei
背景/目的：白细胞介素1 β（IL-1 β）是一种促炎细胞因子，参与牙髓的急性和慢性炎症过程。细胞间粘附分子-1（ICAM-1）和IL-8是两种主要的炎症介质。然而，白细胞介素-1受体相关激酶（IRAKs）信号通路的作用，负责IL-1 β对牙髓cells的炎症效应尚不清楚。方法：培养的人牙髓细胞暴露于IL-1 β与/不预处理和共孵育IRAK 1/4抑制剂或SB 203580（p38抑制剂）。免疫荧光染色检测IRAK-1磷酸化水平。Western blotting检测ICAM-1、IL-8蛋白表达。结果：IL-β刺激牙髓细胞120 min后，IRAK-1的磷酸化水平明显升高; IRAK 1/4抑制剂可减弱IL-1 β诱导的ICAM-1蛋白表达，但对IL-8蛋白表达无影响。IRAK 1/4抑制剂也能抑制IL-1 β诱导的sICAM-1分泌，但不能抑制IL-8分泌。结论：IL-1 β通过刺激IL-8和ICAM-1的表达和分泌，在牙髓炎症反应中起重要作用。此外，在牙髓细胞中，IL-1 β诱导的IL-8和ICAM-1的作用受到IRAK 1/4和p38信号的不同调节。阻断IRAKs和p38信号传导可能在未来控制牙髓炎症。版权所有（C）2018，台湾医学会.出版社：Elsevier Taiwan LLC
Background/purpose: Interleukin 1 beta (IL-1 beta) is a pro-inflammatory cytokine involved in the acute and chronic inflammatory processes of dental pulp. Intercellular adhesion molecule-1 (ICAM-1) and IL-8 are two major inflammatory mediators. However, the role of interleukin-1 receptor-associated kinases (IRAKs) signaling pathways in responsible for the inflammatory effects of IL-1 beta on dental pulp cells is not clear.Methods: Cultured human dental pulp cells were exposed to IL-1 beta with/without pretreatment and co-incubation with IRAK1/4 inhibitor or SB203580 (p38 inhibitor). IRAK-1 phosphorylation was evaluated by immunno fluorescent staining. The protein expression of ICAM-1 and IL-8 were tested by western blotting. The secretion of soluble ICAM-1 (sICAM-1) and IL-8 was measured by enzyme-linked immunosorbant assay (ELISA).Results: IL-beta stimulated IRAK-1 phosphorylation of pulp cells within 120 min of exposure. IRAK1/4 inhibitor attenuated the IL-1 beta-induced ICAM-1, but not IL-8 protein expression. IRAK1/4 inhibitor also prevented the IL-1 beta-induced sICAM-1, but not IL-8 secretion. SB203580 showed little effect on IL-1 beta-induced sICAM-1 secretion, but effectively inhibited its induction of IL-8 secretion in pulp cells.Conclusion: The Results reveal the important role of IL-1 beta in pulpal inflammatory responses via stimulation of IL-8 and ICAM-1 expression and secretion. Moreover, IL-1 beta-induced effects on IL-8 and ICAM-1 are differentially regulated by IRAK1/4 and p38 signaling in dental pulp cells. Blocking of IRAKs and p38 signaling may have potential to control inflammation of dental pulp in the future. Copyright (C) 2018, Formosan Medical Association. Published by Elsevier Taiwan LLC.