ABSTRACT
The enhanced excitability of gastrointestinal smooth muscle following toxin A exposure in vivo probably results from indirect inflammatory factors present in the intestinal wall during infection. Clostridium difficile toxin A is believed to be the causative agent of the subepithelial inflammatory infiltrate in patients, and produces the fluid secretion from the intestine in experimental animals. Independent of the contribution of inflammatory cells, toxin A may induce changes of epithelial cell resistance. The response to toxin A may in turn be amplified through release of several possible inflammatory mediators such as leukotrienes, prostaglandins, interleukins, and neuropeptides from neutrophils, lymphocytes, macrophages, and possibly other cells. The enhanced excitability of gastrointestinal smooth muscle following toxin A exposure in vivo probably results from indirect inflammatory factors present in the intestinal wall during infection. C. difficile toxin A produces fluid secretion and an inflammatory infiltrate in the intestine of experimental animals,4 whereas toxin B is a potent cytotoxin against cultured cells.
