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主要的草花粉过敏原黑麦草Lol p 1与柴油尾气颗粒结合:对哮喘和空气污染的影响。

Major grass pollen allergen Lol p 1 binds to diesel exhaust particles: implications for asthma and air pollution.

作者信息

Knox R B, Suphioglu C, Taylor P, Desai R, Watson H C, Peng J L, Bursill L A

机构信息

Pollen and Allergen Research Group, School of Botany, University of Melbourne, Parkville, Victoria, Australia.

出版信息

Clin Exp Allergy. 1997 Mar;27(3):246-51.

PMID:9088650
Abstract

BACKGROUND

Grass pollen allergens are known to be present in the atmosphere in a range of particle sizes from whole pollen grains (approx. 20 to 55 microns in diameter) to smaller size fractions < 2.5 microns (fine particles, PM25). These latter particles are within the respirable range and include allergen-containing starch granules released from within the grains into the atmosphere when grass pollen ruptures in rainfall and are associated with epidemics of thunderstorm asthma during the grass pollen season. The question arises whether grass pollen allergens can interact with other sources of fine particles, particularly those present during episodes of air pollution.

OBJECTIVE

We propose the hypothesis that free grass pollen allergen molecules, derived from dead or burst grains and dispersed in microdroplets of water in aerosols, can bind to fine particles in polluted air.

METHODS

We used diesel exhaust carbon particles (DECP) derived from the exhaust of a stationary diesel engine, natural highly purified Lol p 1, immunogold labelling with specific monoclonal antibodies and a high voltage transmission electron-microscopic imaging technique.

RESULTS

DECP are visualized as small carbon spheres, each 30-60 nm in diameter, forming fractal aggregates about 1-2 microns in diameter. Here we test our hypothesis and show by in vitro experiments that the major grass pollen allergen, Lol p 1, binds to one defined class of fine particles, DECP.

CONCLUSION

DECP are in the respirable size range, can bind to the major grass pollen allergen Lol p 1 under in vitro conditions and represent a possible mechanism by which allergens can become concentrated in polluted air and thus trigger attacks of asthma.

摘要

背景

已知草花粉过敏原存在于大气中,其颗粒大小范围从完整的花粉粒(直径约20至55微米)到小于2.5微米的较小粒径部分(细颗粒物,PM2.5)。后一种颗粒处于可吸入范围内,包括草花粉在降雨中破裂时从花粉粒内部释放到大气中的含过敏原淀粉颗粒,并且与草花粉季节期间的雷暴哮喘流行有关。问题是草花粉过敏原是否能与其他细颗粒物来源相互作用,特别是空气污染事件期间存在的那些细颗粒物。

目的

我们提出一个假设,即源自死亡或破裂花粉粒并分散在气溶胶中的微水滴中的游离草花粉过敏原分子,可以与污染空气中的细颗粒物结合。

方法

我们使用了源自固定柴油发动机尾气的柴油废气碳颗粒(DECP)、天然高度纯化的黑麦草花粉变应原1(Lol p 1)、用特异性单克隆抗体进行免疫金标记以及高压透射电子显微镜成像技术。

结果

DECP呈现为小碳球,每个直径30 - 60纳米,形成直径约1 - 2微米的分形聚集体。在此我们检验我们的假设,并通过体外实验表明,主要的草花粉过敏原Lol p 1与一类特定的细颗粒物DECP结合。

结论

DECP处于可吸入粒径范围内,在体外条件下能与主要的草花粉过敏原Lol p 1结合,并且代表了一种过敏原可能在污染空气中浓缩从而引发哮喘发作的机制。

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