Cell-Bound IL-8 Increases in Bronchial Epithelial Cells after Arylsulfatase B Silencing due to Sequestration with Chondroitin-4-Sulfate
Cell-Bound IL-8 Increases in Bronchial Epithelial Cells after Arylsulfatase B Silencing due to Sequestration with Chondroitin-4-Sulfate
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DOI：
10.1165/rcmb.2008-0482oc
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发表时间：
2010-01-01
影响因子：
6.4
通讯作者：
Tobacman, Joanne K.
中科院分区：
文献类型：
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作者：
Bhattacharyya, Sumit;Solakyildirim, Kemal;Tobacman, Joanne K.
趋化因子IL-8在人类组织的炎症过程中至关重要，并且IL-8与硫酸化糖胺聚糖的相互作用涉及支气管上皮中炎症反应的修饰。为了确定4-硫酸软骨素（C4 S）在介导IL-8作用中的作用，我们在IB 3 -1和C38支气管上皮细胞系以及正常原代支气管上皮细胞中沉默了从C4 S中去除4-硫酸基团的酶N-乙酰半乳糖胺-4-硫酸酯酶（芳基硫酸酯酶B [AS B]）。当ASB被沉默而IL-8的产生被TNF-α刺激时，在所有细胞系中，ASB活性下降约75%，细胞C4 S含量增加超过7.5 μ g/mg蛋白，细胞结合的IL-8增加超过530 pg/mg蛋白，分泌的IL-8下降超过520 pg/mg蛋白（P
The chemokine IL-8 is critically important in inflammatory processes in human tissues, and IL-8 interactions with sulfated glycosaminoglycans have been implicated in modification of inflammatory responses in bronchial epithelium. To determine the role of chondroitin-4-sulfate (C4S) in mediating effects of IL-8, we silenced the enzyme N-acetylgalactosamine-4-sulfatase (arylsulfatase B [ASB]) that removes the 4-sulfate group from C4S, in the IB3-1 and C38 bronchial epithelial cell lines and in normal primary bronchial epithelial cells. When ASB was silenced and IL-8 production stimulated by exposure to TNF-alpha, ASB activity declined by roughly 75%, cellular C4S content increased by over 7.5 mu g/mg protein, cell-bound IL-8 increased by over 530 pg/mg protein, and secreted IL-8 declined by over 520 pg/mg protein in all cell lines (P