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空气中的真菌会诱导鼻息肉上皮细胞的激活和 Toll 样受体的表达。

Airborne fungi induce nasal polyp epithelial cell activation and Toll-like receptor expression.

机构信息

Department of Otorhinolaryngology, School of Medicine, Catholic University of Daegu, Daegu, South Korea.

出版信息

Int Arch Allergy Immunol. 2010;153(1):46-52. doi: 10.1159/000301578. Epub 2010 Mar 31.

DOI:10.1159/000301578
PMID:20357484
Abstract

BACKGROUND

The nasal epithelium is the first barrier encountered by airborne allergens and is an active participant in airway inflammation. Fungi have been increasingly recognized as important pathogens in sinusitis and airway diseases. The aim of the study was to evaluate fungal protease activity during cytokine production in nasal polyp epithelial cells and to determine the expression of Toll-like receptor (TLR) mRNA by fungi.

METHODS

Nasal polyp epithelial cells were obtained from patients and stimulated with Alternaria and Aspergillus. Interleukin-8 (IL-8) and granulocyte macrophage colony-stimulating factor (GM-CSF) were measured to determine the activation of epithelial cells. Reverse transcriptase polymerase chain reaction for the TLR mRNA expression of the nasal epithelial cells was performed. Cytokine production was inhibited with protease inhibitors and anti-human TLR antibodies.

RESULTS

The fungi enhanced the production of IL-8 and GM-CSF from nasal epithelial cells. When nasal epithelial cells were activated by the fungi, TLR2, TLR3 and TLR4 mRNAs were more strongly expressed than in the nonactivated cells. Cytokine production was inhibited by protease inhibitors and anti-human TLR4 antibodies.

CONCLUSIONS

The results of this study showed that fungi interacted with nasal epithelial cells and enhanced the production of cytokines and TLR mRNA expression. The cytokine production was related to the protease in fungi and TLR4.

摘要

背景

鼻上皮是空气中过敏原首先接触的第一道屏障,是气道炎症的积极参与者。真菌已被越来越多地认为是鼻窦炎和气道疾病的重要病原体。本研究旨在评估真菌蛋白酶活性在鼻息肉上皮细胞细胞因子产生中的作用,并确定真菌 Toll 样受体 (TLR) mRNA 的表达。

方法

从患者中获取鼻息肉上皮细胞,并用交链孢霉和曲霉菌刺激。通过测量白细胞介素-8 (IL-8) 和粒细胞巨噬细胞集落刺激因子 (GM-CSF) 来确定上皮细胞的激活。对鼻上皮细胞的 TLR mRNA 表达进行逆转录聚合酶链反应。用蛋白酶抑制剂和抗人 TLR 抗体抑制细胞因子产生。

结果

真菌增强了鼻上皮细胞产生 IL-8 和 GM-CSF。当真菌激活鼻上皮细胞时,TLR2、TLR3 和 TLR4 mRNA 的表达比非激活细胞更强。蛋白酶抑制剂和抗人 TLR4 抗体抑制细胞因子产生。

结论

本研究结果表明,真菌与鼻上皮细胞相互作用,增强细胞因子的产生和 TLR mRNA 的表达。细胞因子的产生与真菌和 TLR4 中的蛋白酶有关。

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