[Effect of Helicobacter pylori infection on proliferation and apoptosis in stomach antrum in smoking patients].

Peptic ulcer disease develops if the balance between aggressive and defensive factors is destroyed. Among the identified risk factors are Helicobacter pylori infection (Hp), stress, cigarette smoking and taking nonsteroidal anti-inflammatory drugs. However, the exact ulcerogenic mechanism of these factors remains not fully elucidated; yet habitual smoking is the most controversial. The aim of this study was to investigate the influence of cigarette smoking and/or Hp infection on gastric mucosa expression of COX-2, iNOS and proliferation and apoptosis processes (Ki-67 and active caspase 3 expressions, respectively). In smokers without Hp all studied parameters were higher than in nonsmoker without Hp group. Hp infection increases iNOS , COX-2 and active caspase 3 expression. Highest values for iNOS, COX-2 and Ki-67 was observed in smoker with Hp infection group. Hp infection in smokers significantly decrease active caspase 3 expression.