Cell regulation, differentiation and their sequelae in the Helicobacter pylori inflamed and eradicated stomach

Abstract

The issues of cell regulation and turnover in the stomach are of critical importance as they impact directly on the important lesions of erosions, ulcers and cancer, the major complications of H. pylori disease. In uncomplicated H. pylori-associated gastritis and duodenitis an erosion or ulcer results from the inability of the epithelial dynamics adequately to maintain or repair the epithelium at an adequate rate. Further, a persistent long-term increase in epithelial turnover in many organs may predispose to neoplastic sequelae, and in this regard the stomach is no exception. The theory is that increased cell turnover results from increased mitotic activity, and this in turn provides greater opportunities for the production of abnormal cells from which clones may arise, and from which neoplasms may ultimately develop. Further, it is increasingly apparent that while regular cell turnover is associated with a 3–5-day turnover at the surface, and a turnover time measured in months in the pits, that there is a second method of cell degeneration that must be taken into account in epithelial dynamics, which is that of cell apoptosis. Further, the relationships between cell turnover, the inflammatory response and H. pylori itself need to be separated as far as possible. Because H. pylori infection in humans is always associated with at least some degree of chronic inflammatory infiltrate, some of these data necessarily come from animal sources.