Iwaki M, Kamachi K, Heveker N, Konda T
Department of Bacterial and Blood Products, National Institute of Infectious Diseases, Musashimurayama-shi, Tokyo 208-0011, Japan.
Infect Immun. 1999 Jun;67(6):2763-8. doi: 10.1128/IAI.67.6.2763-2768.1999.
The effect of Bordetella pertussis adenylate cyclase toxin (ACT) on platelet aggregation was investigated. This cell-invasive adenylate cyclase completely suppressed ADP (10 microM)-induced aggregation of rabbit platelets at 3 micrograms/ml and strongly suppressed thrombin (0. 2 U/ml)-induced aggregation at 10 micrograms/ml. The suppression was accompanied by marked increase in platelet intracellular cyclic AMP (cAMP) content and was diminished by the anti-ACT monoclonal antibody B7E11. A catalytically inactive point mutant of ACT did not show the suppressive effect. Since an increase of cAMP content is a known cause of platelet dysfunction, these results indicate that the observed platelet inactivation was due to the catalytic activity of ACT through increase of intracellular cAMP.
研究了百日咳博德特氏菌腺苷酸环化酶毒素（ACT）对血小板聚集的影响。这种细胞侵袭性腺苷酸环化酶在3微克/毫升时完全抑制10微摩尔/升二磷酸腺苷（ADP）诱导的兔血小板聚集，在10微克/毫升时强烈抑制0.2单位/毫升凝血酶诱导的聚集。这种抑制伴随着血小板细胞内环磷酸腺苷（cAMP）含量的显著增加，并且被抗ACT单克隆抗体B7E11减弱。ACT的催化无活性点突变体未显示出抑制作用。由于cAMP含量增加是血小板功能障碍的已知原因，这些结果表明观察到的血小板失活是由于ACT通过增加细胞内cAMP的催化活性所致。
