Related Experiment Video
Updated: Aug 19, 2026

One-step Negative Chromatographic Purification of Helicobacter pylori Neutrophil-activating Protein Overexpressed in Escherichia coli in Batch Mode
Published on: June 18, 2016
Inflammation, immunity and vaccines for Helicobacter pylori
Giuseppe Del Giudice1, Pierre Michetti
1Research Center, Chiron Vaccines, Siena, Italy.
Abstract:
Helicobacter pylori causes chronic gastritis in the human stomach, yet only a minority of infected individuals develop peptic ulcer disease, atrophic gastritis, or gastric malignancies. The severity, progression, and consequences of H. pylori infection have been shown to depend on the host genetic background, and in particular on gene polymorphisms affecting the host immune response. Numerous studies published last year brought new information on the mechanisms by which the host genetic make-up modifies the inflammatory and immune responses to H. pylori and the induction of tissue damage secondary to the infection. Novel insights on the regulatory role of H. pylori on the adaptive T-cell response and on its consequences for the persistence of the infection and for the development of vaccines are discussed.
Related Concept Videos
Pathophysiology of Peptic Ulcer Disease: Injurious Factors
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds to M3...
Treating Helicobacter pylori in Peptic Ulcers: Antimicrobial Therapy
Peptic Ulcer Disease II: Pathophysiology
Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.
Peptic Ulcer
Gastritis II: Pathophysiology
Peptic Ulcer Disease II: Pathophysiology

