Japanese cedar pollen upregulates the effector functions of eosinophils.
Japanese cedar pollen upregulates the effector functions of eosinophils.
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DOI：
10.5415/apallergy.2021.11.e26
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发表时间：
2021-07
影响因子：
1.7
通讯作者：
Nagata M
中科院分区：
文献类型：
--
作者：
Miyauchi S;Nakagome K;Noguchi T;Kobayashi T;Ueda Y;Soma T;Nagata M
在日本柳杉花粉 (JCP) 散布季节，鼻炎和哮喘的症状可能会加剧，即使是对 JCP 不敏感的受试者也是如此，这表明先天免疫反应可能有助于这一过程。我们之前报道过屋尘螨直接激活嗜酸性粒细胞的效应功能。类似的机制可能在 JCP 相关的过敏性疾病恶化中发挥作用。旨在研究 JCP 或 JCP 的主要过敏原 Cry j 1 是否可以改变嗜酸性粒细胞的效应功能。用 JCP 或 Cry j 1 刺激从健康供体的外周血中分离出的嗜酸性粒细胞，并使用嗜酸性粒细胞过氧化物酶测定法测量它们与人细胞间粘附分子-1 的粘附力。根据细胞色素 C 的超氧化物歧化酶抑制性还原来测量嗜酸性粒细胞超氧阴离子 (O2 -) 的产生。通过酶联免疫吸附测定来测量细胞培养基中嗜酸性粒细胞衍生的神经毒素的浓度，作为脱颗粒的标记。 JCP和Cry j 1都直接诱导嗜酸性粒细胞粘附、O2 - 的产生以及嗜酸性粒细胞衍生的神经毒素的释放。抗αM和抗β2整联蛋白抗体均阻断JCP和Cry j 1诱导的所有这些嗜酸性粒细胞功能。同样，PAR-2拮抗剂也部分抑制JCP和Cry j 1诱导的所有这些效应子功能。JCP和Cry j 1直接激活嗜酸性粒细胞的功能，并且αMβ2整联蛋白和部分PAR-2都有助于这种激活。因此，JCP诱导的嗜酸性粒细胞活化可能在非致敏患者和JCP致敏患者中过敏性气道疾病的加重中发挥作用。
Symptoms of rhinitis and asthma can be exacerbated during Japanese cedar pollen (JCP)-scattering season, even in subjects who are not sensitized to JCP, suggesting that innate immune responses may contribute to this process. We previously reported that house dust mite directly activates the effector functions of eosinophils. Similar mechanisms may play roles in the JCP-related aggravation of allergic diseases. To investigate whether JCP or Cry j 1, a major allergen of JCP, can modify the effector functions of eosinophils. Eosinophils isolated from the peripheral blood of healthy donors were stimulated with either JCP or Cry j 1, and their adhesion to human intercellular adhesion molecule-1 was measured using eosinophil peroxidase assays. The generation of eosinophil superoxide anion (O2 −) was measured based on the superoxide dismutase-inhibitable reduction of cytochrome C. Concentrations of eosinophil-derived neurotoxin in the cell media were measured by enzyme-linked immunosorbent assay as a marker of degranulation. Both JCP and Cry j 1 directly induced eosinophil adhesiveness, generation of O2 −, and release of eosinophil-derived neurotoxin. Both anti-αM and anti-β2 integrin antibodies blocked all of these eosinophil functions induced by JCP and Cry j 1. Similarly, PAR-2 antagonists also partially suppressed all of these effector functions induced by JCP and Cry j 1. JCP and Cry j 1 directly activate the functions of eosinophils, and both αMβ2 integrin and partly PAR-2 are contributed to this activation. Therefore, JCP-induced eosinophil activation may play a role in the aggravation of allergic airway diseases in nonsensitized patients as well as in JCP-sensitized patients.