Cedar pollens cause severe allergic disease throughout the world. We have previously characterized allergenic pollen glycoproteins from mountain cedar (Juniperus ashei) that bind to allergen-specific immunoglobulin E (IgE). In the present report, we investigated an alternative pathway of mast cell activation by mountain cedar pollen extract through IgE-independent mechanisms. We show that mountain cedar pollen directly induces mast cell serotonin and IL-4 release and enhances release induced by IgE cross-linking. Concomitant with mediator release, high levels of intracellular reactive oxygen species (ROS) were generated, and both ROS and serotonin release were inhibited by anti-oxidants. These findings suggest that alternative mechanisms exist whereby pollen exposure enhances allergic inflammatory mediator release through mechanisms that involve ROS. These mechanisms have the potential for enhancing the allergenic potency of pollens.

中文翻译：

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山雪松花粉诱导不依赖 IgE 的肥大细胞脱粒、IL-4 产生和细胞内活性氧的产生。

雪松花粉在全世界引起严重的过敏性疾病。我们之前已经表征了来自山雪松 (Juniperus ashei) 的过敏性花粉糖蛋白，其与过敏原特异性免疫球蛋白 E (IgE) 结合。在本报告中，我们通过独立于 IgE 的机制研究了山雪松花粉提取物激活肥大细胞的替代途径。我们表明山雪松花粉直接诱导肥大细胞血清素和 IL-4 释放，并增强 IgE 交联诱导的释放。伴随着介质的释放，产生了高水平的细胞内活性氧 (ROS)，并且 ROS 和 5-羟色胺的释放都受到抗氧化剂的抑制。这些发现表明存在其他机制，即花粉暴露通过涉及 ROS 的机制增强过敏性炎症介质的释放。这些机制有可能增强花粉的致敏效力。