Interaction between hyperosmolar and IgE-mediated histamine release from basophils and mast cells.

Interaction between hyperosmolar and IgE-mediated histamine release from basophils and mast cells.
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DOI:
10.1164/arrd.1984.130.1.86
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发表时间:
1984
期刊:
The American review of respiratory disease
影响因子:
--
通讯作者:
P. Eggleston;A. Kagey-sobotka;R. Schleimer;L. Lichtenstein
P. Eggleston;A. Kagey-sobotka;R. Schleimer;L. Lichtenstein
中科院分区:
其他
文献类型:
--
作者:
P. Eggleston;A. Kagey-sobotka;R. Schleimer;L. Lichtenstein

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由于高渗和IgE依赖性刺激可能会遇到在气道中,因为高渗引起组胺释放嗜碱性粒细胞,我们研究了2刺激对人肺肥大细胞的影响。将通过酶消化人肺制备的肥大细胞悬浮在用甘露醇制成的高渗缓冲液中。在高于360 mOsm/kg H2O时观察到显著的组胺释放,在770 mOsm/kg H2O时增加至11.9 +/- 1.0%,并且通过抗IgE协同增强释放。通过在不存在Ca++的情况下暴露于抗IgE而对IgE依赖性刺激无反应的细胞变得对高渗刺激明显更敏感,并且在单独的高渗缓冲液中释放多达32 +/-2%的组胺。抗原诱导的组胺释放从嗜碱性粒细胞的过敏捐助者也协同增强缓冲液中超过460 mOsm/kg H2O。这些数据表明,免疫和非免疫刺激可能相互作用,人肺肥大细胞能够介质释放时,暴露于渗透压,可能发生在气道,特别是在过度换气。高渗介质释放是运动诱导的过度换气可能诱发哮喘的一种合理机制。
Because both hyperosmolar and IgE-dependent stimuli may be encountered in the airway, and because hyperosmolarity causes histamine release in basophils, we examined the effects of the 2 stimuli on human lung mast cells. Mast cells prepared by enzymatic digestion of human lung were suspended in buffers made hyperosmolar with mannitol. Significant histamine release was seen above 360 mOsm/kg H2O, increasing to 11.9 +/- 1.0% at 770 mOsm/kg H2O, and release was synergistically enhanced by anti-IgE. Cells that had been rendered unresponsive to IgE-dependent stimuli by exposure to anti-IgE in the absence of Ca++ became markedly more responsive to hyperosmolar stimulation, and released as much as 32 +/- 2% histamine in hyperosmolar buffers alone. Antigen-induced histamine release from the basophils of allergic donors was also synergistically enhanced in buffers above 460 mOsm/kg H2O. These data show that immunologic and nonimmunologic stimuli may interact, and that human lung mast cells are capable of mediator release when exposed to osmolarities that may occur in the airway, especially during hyperventilation. Hyperosmolar mediator release is a plausible mechanism by which exercise-induced hyperventilation might induce asthma.