page_title: Helicobacter pylori
section_title: Adaptation to the stomach
hierarchical_section_title: Helicobacter pylori / Pathophysiology / Adaptation to the stomach
caption_attribution_description: English: A team of researchers from Boston University, Harvard Medical School and Massachusetts Institute of Technology have shown that the bacterium that causes human stomach ulcers uses a clever biochemical strategy to alter the physical properties of its environment, allowing it to move and survive and further colonize its host.Contact with stomach acid keeps the mucin lining the epithelial cell layer in a spongy gel-like state. This consistency is impermeable to the bacterium Heliobacter pylori. However, the bacterium releases urease which neutralizes the stomach acid. This causes the mucin to liquefy, and the bacterium can swim right through it. Read more about this research. Illustration Credit: Zina Deretsky, National Science Foundation Visit NSF’s Multimedia Gallery, at www.nsf.gov/news/mmg, for more images, and for video.
context_page_description: Helicobacter pylori, previously known as Campylobacter pylori, is a gram-negative, helically-shaped, microaerophilic bacterium usually found in the stomach. Its helical shape is thought to have evolved in order to penetrate the mucoid lining of the stomach and thereby establish infection. The bacterium was first identified in 1982 by Australian doctors Barry Marshall and Robin Warren. H. pylori has been associated with the mucosa-associated lymphoid tissue in the stomach, esophagus, colon, rectum, or tissues around the eye, and of lymphoid tissue in the stomach.
  H. pylori infection usually has no symptoms but sometimes causes gastritis or ulcers of the stomach or first part of the small intestine. The infection is also associated with the development of certain cancers occurring in less than 20% of cases. Many investigators have suggested that H. pylori causes a wide range of other diseases. The bacterial infection has also been proposed to have protective effects for its hosts against infections by other pathogens, asthma, obesity, celiac disease, inflammatory bowel disease, rhinitis, atopic dermatitis, gastroesophageal reflux disease, and esophageal cancer.
context_section_description: To avoid the acidic environment of the interior of the stomach (lumen), H. pylori uses its flagella to burrow into the mucus lining of the stomach to reach the epithelial cells underneath, where it is less acidic. H. pylori is able to sense the pH gradient in the mucus and move towards the less acidic region (chemotaxis). This also keeps the bacteria from being swept away into the lumen with the bacteria's mucus environment, which is constantly moving from its site of creation at the epithelium to its dissolution at the lumen interface.
  H. pylori is found in the mucus, on the inner surface of the epithelium, and occasionally inside the epithelial cells themselves.  It adheres to the epithelial cells by producing adhesins, which bind to lipids and carbohydrates in the epithelial cell membrane. One such adhesin, BabA, binds to the Lewis b antigen displayed on the surface of stomach epithelial cells. H. pylori adherence via BabA is acid sensitive and can be fully reversed by decreased pH. It has been proposed that BabA's acid responsiveness enables adherence while also allowing an effective escape from unfavorable environment at pH that is harmful to the organism. Another such adhesin, SabA, binds to increased levels of sialyl-Lewis x antigen expressed on gastric mucosa.
  In addition to using chemotaxis to avoid areas of low pH, H. pylori also neutralizes the acid in its environment by producing large amounts of urease, which breaks down the urea present in the stomach to carbon dioxide and ammonia. These react with the strong acids in the environment to produce a neutralized area around H. pylori. Urease  knockout mutants are incapable of colonization. In fact, urease expression is not only required for establishing initial colonization but also for maintaining chronic infection.
caption: Diagram showing how H. pylori reaches the epithelium of the stomach
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