Gastritis and Peptic Ulcer Disease Caused by Helicobacter pylori
Introduction
Helicobacter pylori is a Gram-negative, helix-shaped bacterium that is about 3 micrometers long with a diameter of 0.5 micrometers. H. pylori is a microaerophilic bacterium which means that it requires oxygen to function. However, H. pylori requires much lower concentrations of oxygen than those found in our atmosphere. This bacterium contains a hydrogenase which it can use to obtain energy by oxidizing molecular hydrogen (in the form of H2) produced by intestinal bacteria. H. pylori also produces oxidase, catalase, and urease. It has an outer-membrane consisting of phospholipids and lipopolysaccharide which are characteristic of typical Gram-negative bacteria. H. pylori bacteria are known to inhabit various areas of the stomach and duodenum. Infections caused by this bacteria lead to chronic inflammation in the stomach lining (Gastritis). H. pylori infections are also strongly associated to the development of gastric ulcers and even stomach cancer. Although H. pylori is known to cause several problems, over 80% of individuals infected with this bacterium show no symptoms. Over half of all people in the world are thought to harbor this bacterium in their upper gastrointestinal tract.
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Pathogenesis
In order to colonize the stomach H. pylori must survive the acidic pH of its environment. It burrows into the mucus lining that coats the stomach. An H. pylori bacterium has flagella and uses them to move through the stomach lumen and drill into the mucoid lining of the stomach.[1] H. pylori must insert itself near the stomach's epithelial cell layer which is this bacterium’s niche. H. pylori can be found deep in the mucoid lining of the stomach. Mucous is continuously secreted by mucous cells and removed on the luminal side. To avoid being carried into the lumen by the newly formed mucous, H. pylori senses the pH gradient within the mucus layer by chemotaxis and swims away from the acidic contents of the lumen towards the more neutral pH environment of the epithelial cell surface.[2] H. pylori can also be present on the inner surface of the epithelial cells of the stomach. Sometimes the bacterium is even found inside the epithelial cells.[3] H. pylori produces adhesins that bind to membrane-associated lipids and carbohydrates which helps it to adhere to the epithelial cells.[4] The bacterium also produces great quantities of urease, and enzyme located inside and outside of the cell. This enzyme is capable of breaking down urea that is secreted into the stomach. It breaks down the urea into carbon dioxide and ammonia. The ammonia is converted into an ammonium ion by accepting a hydrogen ion from self-ionized water. The left-over hydroxyl ions then react with the carbon dioxide to produce bicarbonate which neutralizes gastric acid. Therefore, H. pylori is dependent upon urease for its survival in the acidic environment found in the stomach. Without the urease enzyme the bacterium would almost inevitably die. The ammonia that is a byproduct of the urease reaction is toxic to epithelial cells of the stomach. H. pylori also produces protease (an enzyme that breaks down proteins), vacuolating cytotoxin A (VacA), and phospholipases (enzymes that hydrolyze phospholipids into fatty acids and other lipophilic substances). All of these products are damaging to the epithelial cells of the stomach.[5]
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References
Broxmeyer, L., Sosnowska, D., Miltner, E., Chacon, O., Wagner, D., McGarvey, J., Barletta, R.G., and Bermudez, L.E. "Killing of Mycobacterium avium and Mycobacterium tuberculosis by a Mycobacteriophage Delivered by a Nonvirulent Mycobacterium: A Model for Phage Therapy of Intracellular Bacterial Pathogens". The Journal of Infectious Diseases. 2002. Volume 186, Number 8. p. 1155-1160.
Clark, J.R. and March, J.B. "Bacteriophages and biotechnology: vaccines, gene therapy and antibacterials". TRENDS in Biotechnology. 2006. Volume 24, Number 5. p. 212-218.
Inal, J.M. "Phage Therapy: a Reappraisal of Bacteriophages as Antibiotics". Archivum Immunologiae et Therapiae Experimentalis. 2003. Volume 51. p. 237-244.
