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细胞表面硫醇的修饰引发人单核细胞系THP-1的激活:可能参与半抗原2,4-二硝基氯苯和硫酸镍的作用。

Modification of cell-surface thiols elicits activation of human monocytic cell line THP-1: possible involvement in effect of haptens 2,4-dinitrochlorobenzene and nickel sulfate.

作者信息

Hirota Morihiko, Suzuki Mie, Hagino Shigenobu, Kagatani Saori, Sasaki Yoshinori, Aiba Setsuya, Itagaki Hiroshi

机构信息

Quality Assessment Center, Shiseido Co., Ltd., Yokohama-shi.

出版信息

J Toxicol Sci. 2009 Apr;34(2):139-50. doi: 10.2131/jts.34.139.

Abstract

Human monocytic cell line THP-1 cells are used as an indicator for in vitro skin sensitization testing. Although p38 mitogen-activated protein kinases (MAPKs) and intracellular redox imbalance play crucial roles in the activation of THP-1 by skin sensitizers, the trigger of cell activation has not been identified. Therefore, we examined whether haptens induce THP-1 maturation directly or indirectly. 2,4-Dinitrochlorobenzene (DNCB), but not dinitrophenol (DNP)-conjugated bovine serum albumin or DNP-conjugated fetal bovine serum, induced CD86 expression. DNCB and nickel sulfate (NiSO4) also induced related changes of cell-surface thiols and phosphorylation of p38 MAPK. However, DNCB is membrane-permeable, and so its direct effect may not be confined to cell membrane proteins. Next, we found that CD86 expression and macrophage inflammatory protein-1beta (MIP-1beta) production were augmented by the membrane-impermeable thiol blocker 5,5'-dithiobis(2-nitrobenzoic acid) (DTNB), and these changes were suppressed by an inhibitor of the p38 MAPK pathway, SB203580. Finally, we confirmed that endocytotic activity for bovine serum albumin (BSA) Alexa Fluor 488 conjugate did not affect cell-surface thiols on THP-1 cells. Thus, our data indicate that the changes of cell-surface thiols are one of the triggers of maturation, and play a key role in activation of THP-1 cells by haptens.

摘要

人单核细胞系THP-1细胞用作体外皮肤致敏试验的指标。虽然p38丝裂原活化蛋白激酶(MAPKs)和细胞内氧化还原失衡在皮肤致敏剂激活THP-1中起关键作用,但细胞激活的触发因素尚未明确。因此,我们研究了半抗原是直接还是间接诱导THP-1成熟。2,4-二硝基氯苯(DNCB)可诱导CD86表达,而二硝基苯酚(DNP)偶联的牛血清白蛋白或DNP偶联的胎牛血清则不能。DNCB和硫酸镍(NiSO4)也可诱导细胞表面硫醇的相关变化以及p38 MAPK的磷酸化。然而,DNCB可透过细胞膜,因此其直接作用可能不限于细胞膜蛋白。接下来,我们发现膜不透性硫醇阻断剂5,5'-二硫代双(2-硝基苯甲酸)(DTNB)可增强CD86表达和巨噬细胞炎性蛋白-1β(MIP-1β)的产生,而这些变化可被p38 MAPK途径抑制剂SB203580抑制。最后,我们证实牛血清白蛋白(BSA)Alexa Fluor 488偶联物的内吞活性不影响THP-1细胞表面的硫醇。因此,我们的数据表明细胞表面硫醇的变化是成熟的触发因素之一,并且在半抗原激活THP-1细胞中起关键作用。

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