Griese M, Merkel G, Feldmann R, Bergfeld I, Reinhardt D
Kinderpoliklinik, Ludwig-Maximilians-Universität, München, Germany.
Eur J Pediatr. 1993 Jul;152(7):585-91. doi: 10.1007/BF01954086.
The influence of childhood pertussis infection and of purified pertussis toxin on histamine release from human basophil leucocytes was investigated. Three different stimuli, the peptide N-formyl-Met-Phe (NFMP), anti-IgE, and the calciumionophore A23187 were used to challenge the cells. When NFMP was the stimulus, histamine release in the control group (age 0.5-17 years) increased in an age-dependent fashion, whereas anti-IgE and A23187 stimulated release did not vary with age. During the convulsive state of pertussis infection there was a significant reduction of histamine release in response to 10 microM NFMP (from 9.5 +/- 1.4 [n = 21] to 6.7 +/- 1.5 [n = 19], P < 0.05) and in response to 800 and 80 U/ml anti-IgE (from 28.5 +/- 5 [n = 19] to 16.3 +/- 5 [n = 13], P < 0.05, and from 6.9 +/- 1.7 [n = 16] to 2 +/- 0.8 [n = 13], P < 0.01), whereas histamine release stimulated by A23187 was unchanged compared to release in control children. In vitro pretreatment of basophils from healthy children and adults with pertussis toxin also inhibited histamine release. When NFMP was the stimulus, release was completely blocked by pertussis toxin with an IC50 of about 11 ng/ml, whereas anti-IgE stimulated release was only inhibited by 20%-30% and release induced by A23187 was reduced to 40%-50% by toxin treatment. In conclusion we have demonstrated a functional impairment of histamine release during the convulsive state of pertussis and that this inhibition is likely to be mediated by pertussis toxin.
研究了儿童期百日咳感染及纯化百日咳毒素对人嗜碱性白细胞组胺释放的影响。使用三种不同的刺激物,即肽N-甲酰基-蛋氨酸-苯丙氨酸(NFMP)、抗IgE和钙离子载体A23187对细胞进行刺激。当以NFMP作为刺激物时,对照组(年龄0.5 - 17岁)的组胺释放呈年龄依赖性增加,而抗IgE和A23187刺激的释放则不随年龄变化。在百日咳感染的惊厥状态下,对10微摩尔NFMP的组胺释放显著减少(从9.5±1.4 [n = 21]降至6.7±1.5 [n = 19],P < 0.05),对800和80 U/ml抗IgE的组胺释放也显著减少(从28.5±5 [n = 19]降至16.3±5 [n = 13],P < 0.05,以及从6.9±1.7 [n = 16]降至2±0.8 [n = 13],P < 0.01),而与对照儿童相比,A23187刺激的组胺释放未改变。用百日咳毒素对健康儿童和成人的嗜碱性粒细胞进行体外预处理也抑制了组胺释放。当以NFMP作为刺激物时,百日咳毒素完全阻断释放,IC50约为11 ng/ml,而抗IgE刺激的释放仅被抑制20% - 30%,毒素处理使A23187诱导的释放减少至40% - 50%。总之,我们证明了百日咳惊厥状态下组胺释放存在功能损害,且这种抑制可能由百日咳毒素介导。