Fumarola D, Miragliotta G, Palma R, Panaro A
G Batteriol Virol Immunol. 1977 Jan-Jun;70(1-6):28-33.
In a previous report it has been shown that enterotoxin preparations (cholera and E. Coli) able to activate adenylatecyclase system, abrogated platelet aggregation induced by ADP. In the present study the same experimental model has been applied to some purified filtrates from Salmonella typhimurium strains. Preparations from 986 and TLM (invasive strains causing also fluid secretion) interfere with platelet aggregation, while 1027 strain (invasive but not evoking fluid secretion) didn't show such effect. It has been argued, as Sandefur and Peterson have demonstrated with different experimental models, that the system of platelet aggregation induced by ADP is valid for some strains of Salmonella typhimurium, which act with a mechanism partially involving adenylatecyclase system (i.g. cholera-like).
在之前的一份报告中已经表明，能够激活腺苷酸环化酶系统的肠毒素制剂（霍乱和大肠杆菌）可消除由ADP诱导的血小板聚集。在本研究中，相同的实验模型已应用于鼠伤寒沙门氏菌菌株的一些纯化滤液。来自986和TLM（也是引起液体分泌的侵袭性菌株）的制剂会干扰血小板聚集，而1027菌株（侵袭性但不引起液体分泌）则未显示出这种作用。正如桑德弗尔和彼得森用不同的实验模型所证明的那样，有人认为，由ADP诱导的血小板聚集系统对某些鼠伤寒沙门氏菌菌株是有效的，这些菌株的作用机制部分涉及腺苷酸环化酶系统（如霍乱样）。
