Gastritis II: Pathophysiology

H. pylori produces urease, an enzyme that breaks down urea into ammonia and carbon dioxide. The ammonia neutralizes gastric acid locally, creating a protective microenvironment where the bacterium can survive and establish infection in the stomach lining.

Urease hydrolyzes urea into ammonia, which buffers the surrounding gastric acid and allows H. pylori to survive long enough to penetrate the mucus layer. This enzyme is essential for the bacterium's initial colonization and establishment in the stomach.

H. pylori induces infected gastric epithelial cells to express PD-L1, which binds to PD-1 receptors on T-cells and suppresses their activity. This immune evasion mechanism allows the bacterium to establish chronic colonization despite the host's immune response.

Persistent H. pylori infection causes chronic inflammation that damages gastric epithelial cells and leads to mucosal atrophy. Over time, this prolonged epithelial damage may progress to intestinal metaplasia, a precancerous change that significantly increases the risk of gastric carcinoma.

H. pylori injects CagA into host cells through a type IV secretion system, where it disrupts cell signaling pathways and tight junctions. This virulence factor promotes inflammation, cellular damage, and increases the risk of gastric malignancy during chronic infection.

H. pylori uses flagella for motility and secretes mucinases to degrade the mucus layer protecting the stomach wall. These adaptations enable the bacterium to reach and adhere to underlying gastric epithelial cells, initiating the inflammatory cascade.

Infected gastric epithelial cells release interleukin-8, a chemokine that recruits immune cells such as neutrophils to the infection site. This amplifies the inflammatory response, contributing to prolonged inflammation and tissue damage characteristic of H. pylori-induced gastritis.