气道上皮细胞功能的调制Pidotimod: NF-kB cytoplasmatic表达式及其核易位与TLR-2表达增加有关。

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的法令,Silvestri M,罗西

气道上皮细胞功能的调制Pidotimod: NF-kB cytoplasmatic表达式及其核易位与TLR-2表达增加有关。

斜体字J Pediatr。2013年5月10日,39:29。doi: 10.1186 / 1824-7288-39-29。

PubMed ID

23663325 (在PubMed

]

文摘

背景:反复呼吸道感染发病率在儿童时期最重要的原因之一。当免疫功能在很大程度上仍然不成熟,气道上皮细胞起着主要的防守作用以来,除了提供一个物理屏障,它也参与了先天和适应性免疫反应。因此研究旨在评估在体外是否pidotimod,合成二肽能够刺激炎症和免疫效应细胞,可以激活参与应对感染支气管上皮细胞功能。方法:BEAS-2B细胞系(人类支气管上皮细胞感染replication-defective腺病毒12-SV40病毒混合)是培养在pidotimod面前,有或没有肿瘤坏死因子(TNF) t1或酵母聚糖评估:1)细胞间粘附分子(ICAM) 1表达,流式细胞术;b) toll样受体(TLR) 2表达和生产,通过免疫荧光流式细胞术和免疫印迹;d)白介素8 (IL)释放,通过酶联免疫吸附试验(ELISA);e)激活extracellular-signal-regulated激酶(ERK1/2)磷酸化和核factor-kappa B (NF-kB)激活,免疫印迹。结果:组成型表达显著上调ICAM-1和引发释放的tnf (ICAM-1)和tnf和酵母聚糖(引发),但不是通过pidotimod。相比之下,增加TLR-2表达式被发现后接触pidotimod 10和100杯/毫升(p < 0.05)和100年协会pidotimod杯/毫升+ tnf (p < 0.05)。免疫印迹分析证实,本构TLR-2表达接触所有的刺激后显著增加。 Finally, while a remarkable inhibition of TNF-alpha -induced ERK1/2 phosphorylation was observed in the presence of pidotimod, both TNF-alpha and pidotimod were effective in inducing NF-kB protein expression in the cytoplasm and its nuclear translocation. CONCLUSION: Through different effects on ERK1/2 and NF-kB, pidotimod was able to increase the expression of TLR-2 proteins, surface molecules involved in the initiation of the innate response to infectious stimuli. The lack of effect on ICAM-1 expression, the receptor for rhinovirus, and on IL-8 release, the potent chemotactic factor for neutrophils (that are already present in sites of infection), may represent protective functions. If confirmed in vivo, these activities may, at least in part, clarify the mechanism of action of this molecule at airway level.

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药物

Pidotimod