Pathogenesis (development of disease)
The bacterium Helicobacter pylori produces the enzyme urease. This hydrolyzes urea in the stomach to ammonia, which in turn neutralizes gastric acid. This allows the bacterium to survive in the acidic environment of the stomach. It colonizes the mucosa (lining) of the stomach, causing it to lose its natural protective barrier. These areas are then no longer protected from the aggressive gastric acid. Inflammatory processes (inflammatory reactions) of the gastric mucosa occur, which can lead to the formation of ulcers.
The immune system reacts to the bacterium but cannot fight it in the stomach. It is thought that the sustained activation of the immune system is ultimately responsible for the development of the diseases caused by Helicobacter pylori.
During the course of infection, Helicobacter pylori spreads from the antral mucosa (lower area in front of the gastric outlet, the junction with the duodenum) ascending (“ascending”) toward the corpus (centrally located body of the stomach, which makes up the main part of the organ).
Etiology (causes)
Biographic causes
- Genetic burden
- Toll-like receptor 1 (TLR1) polymorphism as a susceptibility gene (gene that increases “susceptibility” to the disease).
- Socioeconomic factors
- Large families
- Housing situation, especially during childhood
- Hygienic conditions – in developing countries, 80% of the population is infected with the germ.
