Describe how stomach ulcers can develop in some people (but not others) due to the activity of native microorganisms

Question

What will be an ideal response?

Answer 1

In the stomach, there are bacteria that can live there, although they typically colonize areas that have a higher pH than 2 that coats the stomach and protects the stomach lining from the acid. These areas are created by the mucin layer. In the mucin layer, the pH is actually right about 7 and species of Lactobacillus and Heliobacter as well as a yeast in the genus Torulopsis live there.
One of these microbes, Heliobacter pylori, is now known to be the cause of most gastric ulcers. To get to the mucin layer, this bacterium has flagella that propel it through the stomach's acidic liquid. For the bacteria to get to the mucin layer can take a while, even with flagella. To protect it from stomach acid, Heliobacter pylori secretes an enzyme called urease, which cleaves urea into ammonia and CO2. The CO2 diffuses away, the ammonia stays close to the bacterium. It forms a cloud around the bacterium that neutralizes stomach acid in its immediate vicinity. After reaching the mucin layer, the bacteria burrow into the mucin. Here, H. pylori exhibits another interesting adaptation to its human host. The lipopolysaccharide of H. pylori does not elicit the type of intense inflammatory response elicited by the LPS of E. coli or other Gram-negative bacteria. This isn't well understood, but it has to do with a change in the LPS that causes it to mimic an oligosaccharide called the Lewis antigen. The Lewis antigen is found on human cells and helps our immune system recognize self versus non-self cells. This mimicry is the reason why most people who are colonized with H. pylori do not develop ulcers.
For people who do respond to the bacteria, the immune response is not successful at eliminating the bacteria in the mucin layer because the host killer cells can't penetrate it successfully. The ulcer is created by the damage to the gastric mucosa caused by our own immune system. Then HCL and pepsin attach to the stomach wall. Some strains produce a protein toxin called VacA that leads to vacuolation and apoptosis of its host gastric cells. The role of this toxin in ulcer formation is still controversial, but it may make the inflammatory response to the bacteria more severe.
Why some people respond and others don't is a question we don't currently know the answer too. Two possible answers are 1) people differ genetically in their response to H. pylori LPS and 2) some strains cause greater inflammatory response than others.