Donowitz M, Keusch G T, Binder H J
Gastroenterology. 1975 Dec;69(6):1230-7.
Shigella dysenteriae I is one of several bacteria which produces an enterotoxin capable of stimulating intestinal water and electrolyte secretion. Unlike cholera and Escherichia coli enterotoxins which have been shown to increase intracellular cyclic adenosine monophosphate levels in the small intestine, the mechanism by which shigella enterotoxin causes intestinal secretion is not known. To study shigella enterotoxin-stimulated intestinal secretion, rabbit ileal mucosa exposed in vivo to Shigella dysenteriae I enterotoxin was studied in vitro in a modified Ussing chamber. Fluid and electrolyte accumulation occurred in vivo and net sodium secretion was present in vitro in the enterotoxin-exposed tissue in contrast to net sodium absorption in control mucosa. Short-circuit current (Isc) was similar in shigella enterotoxin-exposed tissue compared with control tissue. The increase adenosine monophosphate was similar to enterotoxin-exposed and control mucosa. The addition of glucose resulted in a smaller increment of Isc in shigella enterotoxin-treated tissue. Mucosal cyclic adenosine monophosphate levels in enterotoxin-exposed mucosa did not differ from those of control. These results indicate that the characteristics of rabbit ileal mucosa exposed to shigella enterotoxin and cholera enterotoxin markedly differ, although both produce electrolyte secretion both in vivo and in vitro. These studies further suggest that, in contrast to its role in cholera enterotoxin-induced intestinal secretion, cyclic adenosine monophosphate may not be in the mediator of shigella enterotoxin stimulation of intestinal fluid and electrolyte secretion.
痢疾志贺菌I型是几种能够产生肠毒素的细菌之一，这种肠毒素能够刺激肠道水分和电解质分泌。与霍乱毒素和大肠杆菌肠毒素不同，霍乱毒素和大肠杆菌肠毒素已被证明会增加小肠内细胞内环磷酸腺苷水平，而志贺菌肠毒素引起肠道分泌的机制尚不清楚。为了研究志贺菌肠毒素刺激的肠道分泌，在改良的乌斯辛克氏小室中对体内暴露于痢疾志贺菌I型肠毒素的兔回肠黏膜进行了体外研究。与对照黏膜中的钠净吸收相反，在体内发生了液体和电解质积聚，并且在体外暴露于肠毒素的组织中存在钠净分泌。与对照组织相比，暴露于志贺菌肠毒素的组织中的短路电流（Isc）相似。暴露于肠毒素和对照黏膜中的环磷酸腺苷增加相似。添加葡萄糖后，志贺菌肠毒素处理的组织中Isc的增加较小。暴露于肠毒素的黏膜中的黏膜环磷酸腺苷水平与对照黏膜没有差异。这些结果表明，尽管兔回肠黏膜在体内和体外都产生电解质分泌，但暴露于志贺菌肠毒素和霍乱肠毒素的兔回肠黏膜的特征明显不同。这些研究进一步表明，与环磷酸腺苷在霍乱肠毒素诱导的肠道分泌中的作用相反，环磷酸腺苷可能不是志贺菌肠毒素刺激肠道液体和电解质分泌的介质。
