Helicobacter Pylori Infection Mechanism | Gastric Ulcer скачать в хорошем качестве

Helicobacter Pylori Infection Mechanism | Gastric Ulcer

Helicobacter pylori (H. pylori) is a gram-negative, spiral-shaped bacterium that colonizes the human stomach and is associated with various gastrointestinal diseases, including gastritis, peptic ulcers, and gastric cancer. This video explores the fascinating yet complex mechanisms by which H. pylori infects the stomach lining, evades the immune system, and contributes to disease pathogenesis. 1. Entry and Colonization: H. pylori is primarily transmitted via oral-oral or fecal-oral routes, with contaminated food, water, or direct contact acting as major sources of infection. Upon entry into the stomach, the bacterium faces an extremely acidic environment (pH ~1-2). To survive, it produces urease, an enzyme that hydrolyzes urea into ammonia and carbon dioxide, thereby neutralizing gastric acid in its immediate surroundings. H. pylori uses its flagella to move through the mucus layer that lines the stomach epithelium, allowing it to reach and attach to the epithelial surface. 2. Adhesion to Gastric Epithelium: The bacterium adheres to gastric epithelial cells via adhesins, such as BabA (blood group antigen-binding adhesin) and SabA (sialic acid-binding adhesin), which bind to specific receptors on host cells. These interactions ensure that H. pylori remains anchored in the stomach, resisting natural mucosal clearance mechanisms. 3. Evasion of Host Immune Response: H. pylori has evolved multiple strategies to evade immune detection and destruction. It can modify its surface lipopolysaccharides (LPS) to resemble host molecules, reducing immune recognition. The bacterium also secretes factors that suppress immune cell activation, including VacA (vacuolating cytotoxin A), which disrupts T-cell function and induces apoptosis in host cells. Additionally, H. pylori can downregulate antimicrobial peptide expression, further enhancing its survival. 4. Toxin Production and Pathogenesis: CagA (Cytotoxin-associated gene A): Some H. pylori strains possess the cag pathogenicity island (cagPAI), which encodes a type IV secretion system that injects CagA into host cells. CagA disrupts signaling pathways, leading to increased inflammation and cellular changes that may contribute to gastric cancer development. VacA (Vacuolating Cytotoxin A): This toxin forms pores in host cell membranes, alters ion balance, and induces apoptosis, contributing to tissue damage. Induction of Inflammation: H. pylori infection triggers the release of pro-inflammatory cytokines (IL-8, IL-6, TNF-α), leading to chronic gastritis and ulcer formation. 5. Chronic Infection and Disease Progression: Long-term colonization results in persistent inflammation, which may lead to peptic ulcers or more severe complications such as gastric atrophy and intestinal metaplasia. The persistent immune response and cellular damage increase the risk of gastric cancer in susceptible individuals.