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健康人吸入(1→3)-β-D-葡聚糖后的效应。

Effects after inhalation of (1-->3)-beta-D-glucan in healthy humans.

作者信息

Thorn J, Beijer L, Rylander R

机构信息

Department of Environmental Medicine, Göteborg University, Sweden.

出版信息

Mediators Inflamm. 2001 Aug;10(4):173-8. doi: 10.1080/09629350124119.

Abstract

BACKGROUND AND AIM

This study was performed to assess the effects of an exposure to a pure (1-->3)-beta-D-glucan, a cell wall component of fungi, plants and certain bacteria.

METHODS

Twenty-one healthy subjects inhaled saline or (1-->3)-beta-D-glucan suspended in saline in a random, double-blind, cross-over design. They were examined before exposure and 24 and 72h afterwards with spirometry, blood sampling and collection of induced sputum. Differential cell counts and eosinophilic cationic protein (ECP) were determined in blood and sputum, and myeloperoxidase (MPO), tumour necrosis factor-alpha (TNF-alpha), and interleukin (IL)-8 and IL-10 were determined in sputum supernatants. TNF-alpha was determined after cultivation of blood mononuclear cells.

RESULTS

In sputum, inhalation of saline caused a significant increase in ECP and TNF-alpha. (1-->3)-beta-D-Glucan inhalation caused a further increase in these cytokines, although not statistically significantly different from the increase induced by inhalation of saline alone. In blood, the number of eosinophils was significantly decreased 72 h after the challenge with (1-->3)-beta-D-glucan. This effect was not found after the inhalation of saline alone. TNF-alpha production from stimulated blood mononuclear cells was significantly decreased 72 h after the (1-->3)-beta-D-glucan inhalation as compared with the increase induced by saline inhalation.

CONCLUSIONS

The results suggest that (1-->3)-beta-D-glucan causes a different type of response as compared with inflammatory agents such as bacterial endotoxin that cause a neutrophil-dominated inflammatory response.

摘要

背景与目的

本研究旨在评估暴露于纯(1→3)-β-D-葡聚糖(一种真菌、植物及某些细菌的细胞壁成分)的影响。

方法

21名健康受试者采用随机、双盲、交叉设计吸入盐水或盐水中悬浮的(1→3)-β-D-葡聚糖。在暴露前以及暴露后24小时和72小时对他们进行肺量计检查、采血及诱导痰收集。测定血液和痰液中的细胞分类计数及嗜酸性阳离子蛋白(ECP),并测定痰液上清液中的髓过氧化物酶(MPO)、肿瘤坏死因子-α(TNF-α)、白细胞介素(IL)-8和IL-10。在血液单核细胞培养后测定TNF-α。

结果

在痰液中,吸入盐水导致ECP和TNF-α显著增加。吸入(1→3)-β-D-葡聚糖使这些细胞因子进一步增加,尽管与单独吸入盐水所致的增加相比无统计学显著差异。在血液中,用(1→3)-β-D-葡聚糖激发后72小时嗜酸性粒细胞数量显著减少。单独吸入盐水后未发现此效应。与吸入盐水所致的增加相比,吸入(1→3)-β-D-葡聚糖后72小时刺激的血液单核细胞产生的TNF-α显著减少。

结论

结果表明,与引起以中性粒细胞为主的炎症反应的炎症因子(如细菌内毒素)相比,(1→3)-β-D-葡聚糖引起的反应类型不同。

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