Takaishi T, Morita Y, Hirai K, Yamaguchi M, Yokota T, Arai K, Ito K, Miyamoto T
Department of Medicine and Physical Therapy, Faculty of Medicine, University of Tokyo, Japan.
Int Arch Allergy Immunol. 1992;98(3):205-10. doi: 10.1159/000236186.
In this study, we have attempted to determine whether mouse peritoneal mast cells released histamine in response to IL-3. Recombinant mouse (m)IL-3 induced histamine release from mouse peritoneal mast cells in a dose-dependent fashion. Histamine release did not occur in the absence of phosphatidyl serine (PS), and was dependent on PS concentrations. The release was 14.3 +/- 3.8 and 43.5 +/- 11.5% (mean +/- SEM, n = 5) at 1 nM IL-3 in the presence of 10 and 20 micrograms/ml of PS. Calcium was required for the response, and in the absence of calcium, significant histamine release was not observed. The kinetics were slower than those of anti-IgE-induced response. IL-3-induced histamine release reached a peak within 15 min, while that by anti-IgE reached 80% of the maximum in 3 min. Lower concentrations of IL-3, which failed to directly induce histamine release, did not enhance anti-IgE-induced histamine release. Other cytokines, including mIL-4, mIL-5, m-granulocyte-macrophage colony-stimulating factor, human (h)IL-1 alpha, hIL-1 beta and hIL-8, neither induced histamine release nor enhanced anti-IgE induced histamine release. IL-4 had no capacity to enhance IL-3-induced histamine release. These results suggest that locally produced IL-3 might modulate mast cell-related inflammation through histamine release from mast cells.
在本研究中，我们试图确定小鼠腹膜肥大细胞是否会响应白细胞介素-3（IL-3）而释放组胺。重组小鼠（m）IL-3 以剂量依赖的方式诱导小鼠腹膜肥大细胞释放组胺。在没有磷脂酰丝氨酸（PS）的情况下不会发生组胺释放，且其释放依赖于 PS 的浓度。在存在 10 和 20 微克/毫升 PS 的情况下，1 纳摩尔 IL-3 时的释放率分别为 14.3±3.8%和 43.5±11.5%（平均值±标准误，n = 5）。该反应需要钙离子，在没有钙离子的情况下，未观察到显著的组胺释放。其动力学比抗 IgE 诱导的反应要慢。IL-3 诱导的组胺释放在 15 分钟内达到峰值，而抗 IgE 诱导的组胺释放在 3 分钟内达到最大值的 80%。未能直接诱导组胺释放的较低浓度的 IL-3 不会增强抗 IgE 诱导的组胺释放。其他细胞因子，包括 mIL-4、mIL-5、m-粒细胞-巨噬细胞集落刺激因子、人（h）IL-1α、hIL-1β和 hIL-8，既不诱导组胺释放，也不增强抗 IgE 诱导的组胺释放。IL-4 没有增强 IL-3 诱导的组胺释放的能力。这些结果表明，局部产生的 IL-3 可能通过肥大细胞释放组胺来调节与肥大细胞相关的炎症。
