Harville B A, Dreyfus L A
Division of Cell Biology and Biophysics, School of Biological Sciences, University of Missouri-Kansas City 64110, USA.
Peptides. 1996;17(3):363-6. doi: 10.1016/0196-9781(96)00033-2.
Heat-stable enterotoxin b (STb) of Escherichia coli is a 48-amino acid basic, disulfide-bonded peptide that causes intestinal secretion in experimental animal models. Recent evidence suggests that the in vivo mechanism of STb action involves release of 5-hydroxytryptamine (5-HT) and production of prostaglandin E2 (PGE2). Here we show STb-mediated release of 5-HT from rat basophilic leukemic cells (RBL-2H3), a mast cell line model used extensively to study 5-HT release. Increasing concentrations of biologically active STb resulted in a dose-dependent release of 5-HT from RBL-2H3 cells. In contrast to these results, reduced and alkylated STb had no effect on 5-HT release. Release of 5-HT from RBL-2H3 cells was independent of extracellular calcium ions and did not involve changes in the intracellular concentration of free Ca2+. In addition, pertussis toxin treatment completely blocked 5-HT release, indicating a role for a pertussis toxin-sensitive G-protein in the mechanism of 5-HT release from this cell type.
大肠杆菌的热稳定肠毒素b（STb）是一种由48个氨基酸组成的碱性、有二硫键的肽，可在实验动物模型中引起肠道分泌。最近的证据表明，STb作用的体内机制涉及5-羟色胺（5-HT）的释放和前列腺素E2（PGE2）的产生。在此，我们展示了STb介导的大鼠嗜碱性白血病细胞（RBL-2H3，一种广泛用于研究5-HT释放的肥大细胞系模型）释放5-HT的过程。生物活性STb浓度的增加导致RBL-2H3细胞中5-HT呈剂量依赖性释放。与这些结果相反，还原和烷基化的STb对5-HT释放没有影响。RBL-2H3细胞释放5-HT与细胞外钙离子无关，且不涉及细胞内游离Ca2+浓度的变化。此外，百日咳毒素处理完全阻断了5-HT释放，表明百日咳毒素敏感的G蛋白在这种细胞类型释放5-HT的机制中发挥作用。
