Warner J A, Yancey K B, MacGlashan D W
J Immunol. 1987 Jul 1;139(1):161-5.
We have found that basophils (n = 9) treated with pertussis toxin (1.0 microgram/ml) fail to respond to a subsequent challenge with either 1.0 microM f-Met peptide (p less than 0.0005) or 0.24 microgram/ml of C5a (p less than 0.0005) although their responses to anti-IgE (0.1 microgram/ml) and A23187 (1.0 microgram/ml) were unaltered. These results were confirmed in purified (average purity = 89 +/- 3%) basophils (n = 4). Leukotriene C4 release was also reduced to 15 +/- 5% of control (p less than 0.005) when pertussis toxin-treated basophils were exposed to 1.0 microM f-Met peptide, although no inhibition was noted when anti-IgE or A23187 were used as the stimuli. The effect of pertussis toxin on basophils appears to be independent of the presence of contaminating mononuclear cells. We found that pertussis toxin inhibited f-Met peptide-induced histamine release regardless of the magnitude of the stimulus (0.01 microM to 1.0 microM f-Met peptide), although anti-IgE-induced release was unaffected over a dose-response curve. The effect of pertussis toxin was found to be both time- and concentration-dependent. The maximum effects were obtained after a 3-hr incubation with 1 microgram/ml of toxin. Lower (0.01 to 0.05 microgram/ml) concentrations of toxin or shorter (30 to 60 min) incubation periods did not significantly (p greater than 0.05) inhibit mediator release.
我们发现，用百日咳毒素（1.0微克/毫升）处理的嗜碱性粒细胞（n = 9），在随后受到1.0微摩尔f - 甲硫氨酸肽（p < 0.0005）或0.24微克/毫升C5a（p < 0.0005）刺激时无反应，尽管它们对抗IgE（0.1微克/毫升）和A23187（1.0微克/毫升）的反应未改变。这些结果在纯化的（平均纯度 = 89 ± 3%）嗜碱性粒细胞（n = 4）中得到证实。当用百日咳毒素处理的嗜碱性粒细胞暴露于1.0微摩尔f - 甲硫氨酸肽时，白三烯C4释放也降至对照的15 ± 5%（p < 0.005），但当用抗IgE或A23187作为刺激物时未观察到抑制作用。百日咳毒素对嗜碱性粒细胞的作用似乎与污染的单核细胞的存在无关。我们发现，无论刺激强度（0.01微摩尔至1.0微摩尔f - 甲硫氨酸肽）如何，百日咳毒素均抑制f - 甲硫氨酸肽诱导的组胺释放，尽管抗IgE诱导的释放在剂量反应曲线上未受影响。发现百日咳毒素的作用具有时间和浓度依赖性。用1微克/毫升毒素孵育3小时后获得最大效应。较低浓度（0.01至0.05微克/毫升）的毒素或较短的孵育时间（30至60分钟）未显著（p > 0.05）抑制介质释放。
