Apoptosis in Helicobacter pylori gastritis and residual gastritis after distal gastrectomy.

Background/aims: Active gastritis, accelerated cell turnover followed by apoptosis, DNA damage and hyperplasia are often seen in the anastomosis area after gastrectomy. Recently, it has been reported that H. pylori induces apoptosis on gastric cells. Until now, the surgical effect itself and H. pylori infection have not been well differentiated as causes of apoptosis associated with gastritis. Our aim is to clarify the relationship of residual gastritis after gastrectomy and H. pylori gastritis.

Methodology: Residual gastritis model using the Mongolian gerbil has been established with microsurgical technique. Residual gastritis with and without H. pylori infection was studied by histopathological examination and quantitated by Rauws' score. Elevation of pH in gastric juice after surgery was confirmed. Stimulation of downstream events leading to apoptosis, cleavage of poly-ADP-ribose polymerase as a result of activation of caspase-3, was evaluated using Western blotting.

Results: Histopathologically, H. pylori infection led to deterioration after surgery. The postoperative Rauws' score with infection was higher than without infection. Cleavage of poly-ADP-ribose polymerase was increased after surgery in gerbils with and without H. pylori infection. Densitometric study showed a greater increase in the animals with H. pylori infection than those without infection that was enhanced after surgery (0.59 vs. 1.04, 0.73 vs. 1.17, respectively).

Conclusions: Apoptosis is increased both in residual gastritis and H. pylori gastritis. Both enterogastric reflux and H. pylori infection may be linked to tumorigenesis in anastomosis sites followed by accelerated epithelial cell turnover followed by apoptosis.