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脂多糖对支气管上皮细胞中S100A8和S100A9蛋白的上调作用。

Up-regulation of S100A8 and S100A9 protein in bronchial epithelial cells by lipopolysaccharide.

作者信息

Henke Markus O, Renner Armin, Rubin Bruce K, Gyves Juliana I, Lorenz Eva, Koo Ja Seok

机构信息

Department of Pulmonary Medicine, Philipps-University Marburg, Marburg, Germany.

出版信息

Exp Lung Res. 2006 Sep;32(8):331-47. doi: 10.1080/01902140600959580.

DOI:10.1080/01902140600959580
PMID:17090475
Abstract

Increased serum levels of the S100A8 (MRP-8) protein have been reported in inflammatory conditions including bacterial infection, arthritis, and cystic fibrosis (CF). This protein is expressed constitutively with S100A9 (MRP-14) in neutrophils and is regulated by inflammatory stimulants. It has been hypothesized that increased inflammatory response to persistent bacterial infection is a major feature of CF lung disease. Therefore, the authors wished to determine the involvement of these two proteins in the innate defense response of the bronchial epithelium to lipopolysaccharide (LPS). Human bronchial epithelial cells (16HBE14o-) and primary bronchial epithelial cells (NHBE) were grown at air-liquid interface (ALI) and stimulated for up to 96 hours with LPS from Pseudomonas aeruginosa. The 16HBE14o- cells responded to LPS with a 2.9-fold increase in S100A8 mRNA production after 12 hours. S100A9 mRNA production was increased by 1.8-fold after 12 hours and 2.9-fold after 24 hours. It was also found that the S100A8 and S100A9 proteins were increased in the secretions of the 16HBE14o- and NHBE cells after LPS stimulation. This finding suggests that S100A8 and S100A9 are involved in the innate defense of the bronchial epithelium.

摘要

在包括细菌感染、关节炎和囊性纤维化(CF)在内的炎症性疾病中,已有报道血清中S100A8(MRP-8)蛋白水平升高。该蛋白在中性粒细胞中与S100A9(MRP-14)组成性表达,并受炎症刺激物调节。据推测,对持续性细菌感染的炎症反应增强是CF肺部疾病的主要特征。因此,作者希望确定这两种蛋白在支气管上皮细胞对脂多糖(LPS)的固有防御反应中的作用。人支气管上皮细胞(16HBE14o-)和原代支气管上皮细胞(NHBE)在气液界面(ALI)培养,并用铜绿假单胞菌的LPS刺激长达96小时。12小时后,16HBE14o-细胞对LPS的反应是S100A8 mRNA产量增加2.9倍。12小时后S100A9 mRNA产量增加1.8倍,24小时后增加2.9倍。还发现,LPS刺激后,16HBE14o-和NHBE细胞分泌物中的S100A8和S100A9蛋白增加。这一发现表明,S100A8和S100A9参与支气管上皮的固有防御。

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