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Living Dangerously: How Helicobacter Pylori Survives In The Human Stomach

Living dangerously: how Helicobacter pylori survives in the human stomach


Montecucco, C.

Article in Nature Reviews Molecular Cell Biology · July 2001


Helicobacter pylori is a GRAM-NEGATIVE BACTERIUM, specialized in the colonization of the human stomach, a unique ecological niche characterized by very acidic pH— a condition lethal for most microbes. H. pylori is so well adapted to this unfriendly environment that, after the first infection, which usually occurs early in life, it establishes a life-long chronic infection. The selection of a niche with no competition and the ability to establish a chronic infection make H. pylori one of the most successful human bacterial parasites, which colonizes more than half of the human population. 


The comparison of H. pylori isolated from patients of different ethnical origin and geographical locations indicates that their nucleotide sequences segregate similarly to those of humans. This suggests that this bacterium was already present in the stomach of humans when they left Africa to colonize the world, and co-evolved with them since then.Hence, it is likely that primitive humans suffered from stomach aches, although the first written reports were made by ancient Greek doctors and gastric ulcers were first described5 in 1586. 


Most infected people are asymptomatic,with moderate inflammation detectable only by biopsy and histology. However, an important minority of them (15–20%) during their life develop severe gastroduodenal pathologies,including stomach and duodenal ulcers, ADENOCARCINOMAS and stomach LYMPHOMAS.The different outcomes of the infection are believed to be substantially influenced by an excessive or inappropriate reaction of the host, by bacterial polymorphisms and by environmental factors. 


The successful life-lasting colonization of the human stomach by H. pylori is achieved through a combination of factors, which address the different challenges presented by the harsh environment H. pylori synthesizes a urease to buffer the pH of its immediate surroundings within the stomach. Its helicoidal shape and the action of flagella allow it to cross the thick layer of MUCUS lining the stomach. H. pylori then binds to LEWIS ANTIGENS present on host gastric cells, and it secretes factors that attract and stimulate inflammatory cells, as well as the multifunctional toxin VacA. Last, the presence of the cag pathogenicity island, a 40-kb DNA that encodes a type IV secretion system, seems to be necessary for optimal fitness of the bacterium and the appearance of pathogenic traits.




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