Virulence and pathogenicity of Helicobacter pylori.
H. pylori is a highly virulent organism as evidenced by its low infective dose and widespread high prevalence in human populations. Its virulence is achieved through its ability to survive in a moist environment and its massive urease production which allows it to survive in the acidic gastric juice long enough to colonize the gastric mucus. Gastric colonization is facilitated by cell wall associated lectins which permit the bacterium to bind to gastric mucus and the gastric epithelial cell. Once in this location, H. pylori produces several enzymes which may harm the gastric epithelium, particularly urease (through ammonia generation) and phospholipases A and C. H. pylori also weakens the gastric mucous layer by digesting its glycoproteins and lipids, making the mucus less hydrophobic and more water soluble. Helicobacter pylori attracts phagocytic cells, inducing both acute and chronic inflammation as well as an antibody response. Persistence of H. pylori in the mucosa may be enhanced by its cytotoxin and catalase production, by which it survives after phagocytosis by neutrophils.
Marshall
B J
BJ
Department of Internal Medicine, University of Virginia Health Sciences Center, Charlottesville 22908.
D001427:Bacterial Toxins / Q000378:metabolism; D002374:Catalase / Q000378:metabolism; D005753:Gastric Mucosa / Q000382:microbiology; D016481:Helicobacter Infections / Q000453:epidemiology / Q000382:microbiology*; D016480:Helicobacter pylori / Q000201:enzymology / Q000472:pathogenicity*; D006801:Humans; D009093:Mucus / Q000382:microbiology; D010741:Phospholipases A / Q000378:metabolism; D015995:Prevalence; D010738:Type C Phospholipases / Q000378:metabolism; D014510:Urease / Q000378:metabolism
D001427:Bacterial Toxins; D002374:Catalase; D010741:Phospholipases A; D010738:Type C Phospholipases; D014510:Urease