Coadaptation of Helicobacter pylori and humans: ancient history, modern implications.
Humans have been colonized by Helicobacter pylori for at least 50,000 years and probably throughout their evolution. H. pylori has adapted to humans, colonizing children and persisting throughout life. Most strains possess factors that subtly modulate the host environment, increasing the risk of peptic ulceration, gastric adenocarcinoma, and possibly other diseases. H. pylori genes encoding these and other factors rapidly evolve through mutation and recombination, changing the bacteria-host interaction. Although immune and physiologic responses to H. pylori also contribute to pathogenesis, humans have evolved in concert with the bacterium, and its recent absence throughout the life of many individuals has led to new human physiological changes. These may have contributed to recent increases in esophageal adenocarcinoma and, more speculatively, other modern diseases.
Atherton
John C
JC
Nottingham Digestive Diseases Centre Biomedical Research Unit and Institute of Infection, Immunity and Inflammation, Centre for Biomolecular Sciences, University of Nottingham, Nottingham, United Kingdom. John.Atherton@nottingham.ac.uk
Blaser
Martin J
MJ
D000222:Adaptation, Physiological; D000818:Animals; D000942:Antigens, Bacterial / Q000235:genetics / Q000633:toxicity; D001426:Bacterial Proteins / Q000235:genetics / Q000633:toxicity; D019143:Evolution, Molecular; D014644:Genetic Variation; D016481:Helicobacter Infections / Q000266:history* / Q000276:immunology / Q000382:microbiology; D016480:Helicobacter pylori / Q000235:genetics / Q000276:immunology / Q000472:pathogenicity*; D049672:History, 19th Century; D049673:History, 20th Century; D049674:History, 21st Century; D049690:History, Ancient; D054884:Host-Pathogen Interactions / Q000235:genetics / Q000276:immunology / Q000502:physiology*; D006801:Humans; D006967:Hypersensitivity / Q000209:etiology; D008954:Models, Biological; D010437:Peptic Ulcer / Q000209:etiology / Q000382:microbiology; D013274:Stomach Neoplasms / Q000209:etiology / Q000382:microbiology
D000942:Antigens, Bacterial; D001426:Bacterial Proteins; C074689:VacA protein, Helicobacter pylori; C080866:cagA protein, Helicobacter pylori