A comparison of the osmotic activation of basophils and human lung mast cells.

A comparison of the osmotic activation of basophils and human lung mast cells.
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DOI:
10.1164/arrd.1987.135.5.1043
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发表时间:
2015-05
期刊:
The American review of respiratory disease
影响因子:
--
通讯作者:
P. Eggleston;A. Kagey-sobotka;L. Lichtenstein
P. Eggleston;A. Kagey-sobotka;L. Lichtenstein
中科院分区:
其他
文献类型:
--
作者:
P. Eggleston;A. Kagey-sobotka;L. Lichtenstein

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嗜碱性细胞和肥大细胞在高渗环境中释放组胺。渗透释放与ige依赖性激活有显著不同,在静脉输注高渗性造影剂期间的类过敏反应和运动后哮喘患者遭受的阻塞性发作的病理生理学中可能很重要。为了证实报道的嗜碱性粒细胞和肺肥大细胞渗透激活的差异,系统地比较了两种细胞类型的渗透激活过程。两种细胞均被高渗透性甘露醇、葡萄糖、蔗糖和NaCl激活,但嗜碱性细胞的组胺释放量急剧上升,达到最大值1050 mOsm/kg,而肥大细胞的组胺释放量在700 ~ 750 mOsm/kg时达到最大值。释放在嗜碱性细胞中部分依赖于Ca2+,但在肥大细胞中高度依赖于Ca2+。肥大细胞的释放迅速,基本上在5分钟内完成,而嗜碱性细胞则需要45至60分钟。两种细胞类型的最佳温度均为32℃,并且通过增加细胞内cAMP (PGE2、IBMX和db cAMP)的药物可以增强两种细胞的释放。我们得出结论,嗜碱性细胞和肥大细胞的渗透活化是一个无毒的过程,与ige依赖性组胺释放有很大不同。如果它确实参与了人类疾病的病理生理学,就需要不同的治疗策略来调节这一作用。
Basophils and mast cells release histamine in hyperosmolar environments. Osmotic release differs significantly from IgE-dependent activation and may be important in the pathophysiology of anaphylactoid reactions during intravenous infusions of hyperosmolar radiocontrast dyes and of obstructive attacks suffered by asthmatics after exercise. To confirm reported differences in osmotic activation of basophils and lung mast cells, the process was compared systematically in the 2 cell types. Both cells were activated by hyperosmolar mannitol, glucose, sucrose, and NaCl, but histamine release from basophils rose sharply to a maximum at 1,050 mOsm/kg, whereas mast cells released maximally at 700 to 750 mOsm/kg. Release was partially Ca2+-dependent in basophils but was highly Ca2+-dependent in mast cells. Release in mast cells was rapid and essentially complete by 5 min, whereas 45 to 60 min were required in basophils. The temperature optimum in both cell types was 32 degrees C, and release in both was enhanced by drugs that increase intracellular cAMP (PGE2, IBMX, and db cAMP). We conclude that osmotic activation of basophils and mast cells is a nontoxic process that differs significantly from IgE-dependent histamine release. If it does indeed participate in the pathophysiology of human disease, different treatment strategies will be required to modulate this contribution.