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花粉相关脂质介质诱导人外周血嗜酸性粒细胞的趋化性及活化

Chemotaxis and activation of human peripheral blood eosinophils induced by pollen-associated lipid mediators.

作者信息

Plötz Sabine G, Traidl-Hoffmann Claudia, Feussner Ivo, Kasche Anna, Feser Alexandra, Ring Johannes, Jakob Thilo, Behrendt Heidrun

机构信息

Division of Environmental Dermatology and Allergy GSF/TUM, Center for Allergy and Environment, Technical University Munich, Biedersteiner Strasse 29, 80802 Munich, Germany.

出版信息

J Allergy Clin Immunol. 2004 Jun;113(6):1152-60. doi: 10.1016/j.jaci.2004.03.011.


DOI:10.1016/j.jaci.2004.03.011
PMID:15208598
Abstract

BACKGROUND: Eosinophil accumulation at sites of allergic inflammation is largely regulated by chemokines and lipid mediators released by a variety of cells of the local microenvironment. Recent studies have shown that pollen grains, apart from their function as allergen carriers, are a rich exogenous source of eicosanoid-like lipid mediators that are rapidly released on contact with the aqueous phase and thus may contribute to the generation of local inflammatory responses. OBJECTIVE: Here we analyze the biological activity of pollen-associated lipid mediators (PALMs) on peripheral human blood eosinophils. METHODS: Human eosinophils were coincubated with pollen grains and analyzed by electron microscopy. The lipid mediator composition of aqueous pollen extracts (APEs) was analyzed by HPLC. Human eosinophils were exposed to APEs or lipid fractions from pollen. Effects on eosinophils were tested by transwell migration and surface expression of CD11b. RESULTS: In vitro experiments showed adhesion of eosinophils to Phleum pratense pollen. In chemotaxis assays eosinophils displayed significant directed migration to APEs. HPLC analysis of APEs from Phleum pratense and Betula alba pollen demonstrated the occurrence of linoleic and alpha-linolenic acid as well as their monohydroxylated derivatives. Moreover, total lipid extracts from pollen and RP-HPLC fractions containing monohydroxylated derivatives of linoleic and alpha-linolenic acid induced similar migratory responses, although to a lesser degree than APEs. In addition, APEs and lipid extracts induced up-regulation of CD11b surface expression and secretion of eosinophil cationic protein. APE-induced chemotaxis was blocked by the leukotriene B(4) receptor antagonist LY293111, suggesting that PALMs may serve as ligands for LTB(4) receptors. CONCLUSION: Pollen grains release lipid mediators that recruit and activate eosinophils in vitro. Similar mechanisms may be effective under natural exposure conditions, in which PALMs may play a role in the recruitment of eosinophils to the site of allergic inflammation.

摘要

背景:嗜酸性粒细胞在过敏性炎症部位的聚集很大程度上受局部微环境中多种细胞释放的趋化因子和脂质介质调节。最近的研究表明,花粉粒除了作为过敏原载体的功能外,还是类二十烷酸脂质介质的丰富外源性来源,这些介质在与水相接触时会迅速释放,因此可能有助于局部炎症反应的产生。 目的:在此我们分析花粉相关脂质介质(PALMs)对人外周血嗜酸性粒细胞的生物学活性。 方法:将人嗜酸性粒细胞与花粉粒共同孵育,并通过电子显微镜进行分析。通过高效液相色谱法(HPLC)分析水性花粉提取物(APEs)的脂质介质组成。将人嗜酸性粒细胞暴露于APEs或花粉的脂质组分。通过跨膜迁移和CD11b的表面表达来测试对嗜酸性粒细胞的影响。 结果:体外实验显示嗜酸性粒细胞与早熟禾花粉发生黏附。在趋化性试验中,嗜酸性粒细胞对APEs表现出显著的定向迁移。对早熟禾和白桦花粉的APEs进行HPLC分析表明存在亚油酸和α-亚麻酸及其单羟基化衍生物。此外,花粉的总脂质提取物以及含有亚油酸和α-亚麻酸单羟基化衍生物的反相高效液相色谱(RP-HPLC)组分诱导了相似的迁移反应,尽管程度低于APEs。此外,APEs和脂质提取物诱导了CD11b表面表达上调以及嗜酸性粒细胞阳离子蛋白的分泌。白三烯B4受体拮抗剂LY293111阻断了APEs诱导的趋化作用,表明PALMs可能作为白三烯B4受体的配体。 结论:花粉粒释放脂质介质,在体外募集并激活嗜酸性粒细胞。类似的机制在自然暴露条件下可能有效,其中PALMs可能在将嗜酸性粒细胞募集到过敏性炎症部位中发挥作用。

相似文献

[1]
Chemotaxis and activation of human peripheral blood eosinophils induced by pollen-associated lipid mediators.

J Allergy Clin Immunol. 2004-6

[2]
Lipid mediators from pollen act as chemoattractants and activators of polymorphonuclear granulocytes.

J Allergy Clin Immunol. 2002-5

[3]
Allergen extracts directly mobilize and activate human eosinophils.

Eur J Immunol. 2004-6

[4]
The degree of natural allergen exposure modifies eosinophil activity markers in the circulation of patients with mild asthma.

Allergy. 1996-10

[5]
Immunomodulatory effects of aqueous birch pollen extracts and phytoprostanes on primary immune responses in vivo.

J Allergy Clin Immunol. 2007-8

[6]
CD28 and secretory immunoglobulin A-dependent activation of eosinophils: inhibition of mediator release by the anti-allergic drug, suplatast tosilate.

Clin Exp Allergy. 2004-9

[7]
House dust mite allergen activates human eosinophils via formyl peptide receptor and formyl peptide receptor-like 1.

Eur J Immunol. 2007-7

[8]
Impact of urbanization on the proteome of birch pollen and its chemotactic activity on human granulocytes.

Int Arch Allergy Immunol. 2010

[9]
Responsiveness of eosinophils to aeroallergens may be independent of atopic status.

Scand J Immunol. 2008-4

[10]
The activated eosinophil in allergy and asthma.

Prog Clin Biol Res. 1989

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[9]
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