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首页> 外文期刊>American Journal of Physiology >Eosinophil adhesion to cholinergic nerves via ICAM-1 and VCAM-1 and associated eosinophil degranulation.
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Eosinophil adhesion to cholinergic nerves via ICAM-1 and VCAM-1 and associated eosinophil degranulation.

机译：嗜酸性粒细胞通过ICAM-1和VCAM-1与胆碱能神经的粘附以及相关的嗜酸性粒细胞脱粒。

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摘要

In vivo, eosinophils localize to airway cholinergic nerves in antigen-challenged animals, and inhibition of this localization prevents antigen-induced hyperreactivity. In this study, the mechanism of eosinophil localization to nerves was investigated by examining adhesion molecule expression by cholinergic nerves. Immunohistochemical and functional studies demonstrated that primary cultures of parasympathetic nerves express vascular cell adhesion molecule-1 (VCAM-1) and after cytokine pretreatment with tumor necrosis factor-alpha and interferon-gamma intercellular adhesion molecule-1 (ICAM-1). Eosinophils adhere to these parasympathetic neurones after cytokine pretreatment via a CD11/18-dependent pathway. Immunohistochemistry and Western blotting showed that a human cholinergic nerve cell line (IMR-32) expressed VCAM-1 and ICAM-1. Inhibitory experiments using monoclonal blocking antibodies to ICAM-1, VCAM-1, or CD11/18 and with the very late antigen-4 peptide inhibitor ZD-7349 showed that eosinophils adhered to IMR-32 cells via these adhesion molecules. The protein kinase C signaling pathway is involved in this process as a specific inhibitor-attenuated adhesion. Eosinophil adhesion to IMR-32 cells was associated with the release of eosinophil peroxidase and leukotriene C(4). Thus eosinophils adhere to cholinergic nerves via specific adhesion molecules, and this leads to eosinophil activation and degranulation; this may be part of the mechanism of eosinophil-induced vagal hyperreactivity.
机译：在体内，嗜酸性粒细胞在抗原挑战的动物中定位于气道胆碱能神经，抑制该定位可防止抗原诱导的反应过度。在这项研究中，通过检查胆碱能神经的粘附分子表达来研究嗜酸性粒细胞定位于神经的机制。免疫组织化学和功能研究表明，副交感神经的原代培养物表达血管细胞粘附分子1（VCAM-1），并在用肿瘤坏死因子-α和干扰素-γ细胞间粘附分子1（ICAM-1）进行细胞因子预处理后表达。细胞因子预处理后，嗜酸性粒细胞通过CD11 / 18依赖性途径粘附于这些副交感神经元。免疫组织化学和蛋白质印迹表明，人胆碱能神经细胞系（IMR-32）表达VCAM-1和ICAM-1。使用针对ICAM-1，VCAM-1或CD11 / 18的单克隆封闭抗体以及非常晚的抗原4肽抑制剂ZD-7349进行的抑制实验表明，嗜酸性粒细胞通过这些粘附分子粘附至IMR-32细胞。蛋白激酶C信号转导途径以特异性抑制剂减弱的粘附性参与该过程。嗜酸性粒细胞对IMR-32细胞的粘附与嗜酸性粒细胞过氧化物酶和白三烯C（4）的释放有关。因此，嗜酸性粒细胞通过特定的粘附分子粘附在胆碱能神经上，这导致嗜酸性粒细胞活化和脱粒。这可能是嗜酸性粒细胞引起的迷走神经过度反应机制的一部分。

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