Peptic Ulcer

Peptic ulcers are erosions in the stomach or duodenal lining.

Most of these ulcers are caused by infections of Helicobacter pylori, a Gram-negative, spiral-shaped bacterium.

H. pylori survives the acidic environment of the stomach by producing urease, an enzyme that converts urea in the gastric juices into ammonia.

The ammonia neutralizes the acidity around the bacteria.

The bacteria penetrate the protective mucus layer, attach to epithelial cells, and multiply.

The bacteria also produce virulence factors such as VacA and CagA.

VacA induces apoptosis in epithelial cells, while CagA triggers the release of pro-inflammatory cytokines, attracting neutrophils to the site of infection.

Neutrophils fail to clear bacteria that persist beneath the mucus layer, leading to chronic inflammation.

This inflammation compromises the mucus barrier, exposing epithelial cells to highly acidic gastric juice.

Acid damages these cells and the underlying tissue, creating ulcers.

As the ulcer deepens, damage may extend into blood vessels, causing bleeding and further complications.