Gastritis II: Pathofysiologie

H. pylori-induced gastritis begins with bacterial transmission to the gastric mucosa, commonly via contaminated food or water.

H. pylori survives the stomach's acidic environment by producing urease. Urease hydrolyzes urea into ammonia, neutralizing gastric acid locally and creating a protective microenvironment.

The bacterium then uses its flagella and mucolytic enzymes to penetrate the mucus layer and adhere to gastric epithelial cells.

This attachment initiates an immune response. Macrophages and T-cells attempt to clear the infection, but H. pylori triggers epithelial cells to express programmed death-1 ligand 1, or PD-L1. PD-L1 binds to PD-1 on T-cells, sending inhibitory signals that reduce their activity and allow immune evasion.

Simultaneously, H. pylori triggers interleukin-8 secretion, attracting neutrophils and amplifying inflammation.

H. pylori injects virulence factors like the Cytotoxin-associated gene A into host cells. This disrupts cell signaling and tight junctions, contributing to prolonged inflammation and gastritis.