How does Helicobacter pylori infection contribute to the development of stomach ulcers?

Sourav PanNovember 9, 2024

Answered

Helicobacter pylori (H. pylori) infection is a significant contributor to the development of stomach ulcers, including both gastric and duodenal ulcers. The relationship between H. pylori and ulcer formation involves several mechanisms that disrupt the protective lining of the stomach and increase acid secretion. Here’s how H. pylori infection leads to the development of ulcers:

1. Colonization and Inflammation

• Mucosal Colonization: H. pylori is a gram-negative bacterium that can survive in the acidic environment of the stomach by producing enzymes such as urease, which neutralizes gastric acid. This allows it to colonize the gastric epithelium, particularly in areas where the mucosal barrier is compromised.
• Chronic Gastritis: The presence of H. pylori triggers an inflammatory response in the gastric mucosa, leading to chronic gastritis. This inflammation is characterized by an infiltration of immune cells, which can damage the epithelial lining and disrupt its integrity, making it more susceptible to injury from gastric acid and digestive enzymes.

2. Increased Acid Secretion

• Gastrin Production: H. pylori infection often results in increased production of gastrin, a hormone that stimulates acid secretion from parietal cells in the stomach. This occurs because H. pylori-induced inflammation impairs the normal feedback mechanisms that regulate gastrin release. Specifically, when acid levels are high, somatostatin (which inhibits gastrin secretion) is not released adequately, leading to further increases in gastric acid production.
• Acid Hypersecretion: The hypersecretion of gastric acid creates a more acidic environment in the stomach and duodenum, which can overwhelm the protective mechanisms of the gastric mucosa and contribute to ulcer formation. This increased acid load can damage the epithelial cells directly and lead to erosion of the mucosal barrier.

3. Disruption of Mucosal Defense

• Damage to Mucous Layer: H. pylori can produce various virulence factors, such as cytotoxin-associated gene A (CagA) and vacuolating cytotoxin (VacA), which can disrupt the protective mucous layer of the stomach lining. This disruption allows gastric acid and pepsin to penetrate deeper into the tissue, leading to ulceration.
• Epithelial Injury: The combination of increased acid secretion and impaired mucosal defenses results in epithelial injury. Over time, this injury can lead to the formation of ulcers as the underlying tissues become exposed to harsh gastric contents.

4. Ulcer Development

• Peptic Ulcer Disease (PUD): The ongoing cycle of inflammation, increased acid secretion, and mucosal damage can lead to peptic ulcer disease (PUD). While not all individuals infected with H. pylori develop ulcers, those with additional risk factors—such as genetic predisposition or use of nonsteroidal anti-inflammatory drugs (NSAIDs)—are at a higher risk.
• Healing and Recurrence: Eradication of H. pylori through antibiotic therapy often leads to healing of existing ulcers and reduces the risk of recurrence by restoring normal gastric physiology and reducing acid secretion.