Lipolytic activity of Campylobacter pylori: effect of colloidal bismuth subcitrate (De-Nol)

Infection by Campylobacter pylori appears to play a major role in the etiology of gastric disease, but the nature of impairment evoked by this pathogen in gastric mucosal defense is not well understood. We present here evidence that the extracellular material elaborated by this microorganism exhibits lipolytic activity capable of gastric mucosal lipid degradation. The colonies of bacteria, cultured from antral mucosal biopsy specimens of patients undergoing endoscopy, were washed with saline, passed through a sterilization filter, and the filtrate was examined for lipase and phospholipase activities. By following the degradation of glycerol trioleate and dipalmitoyl phosphatidylcholine, we established the presence of lipase and phospholipase A enzymes. The major product of the triglyceride degradation was glycerol monooleate, while lysophosphatidylcholine resulted from the degradation of phosphatidylcholine. The lipolytic activity of C. pylori filtrate was inhibited by an antiulcer drug, De-Nol, which at 150 micrograms/ml caused a 21% reduction in lipase activity and a 60% reduction in the activity of phospholipase A. The results suggest that De-Nol is capable of preventing degradation of mucosal lipids by C. pylori lipases and, hence, helps to preserve the mucosal integrity.