Nobel Prize Winners May Help Stamp Out Stomach Ulcers

Over 25 million Americans will suffer from an ulcer at some point during their lifetime, according to the Center for Disease Control.

If you think, like many medical experts once thought, that bacterium cannot live in the acidic juices of the stomach, think again.

Drs. Barry Marshall and Robin Warren of Australia discovered that helicobacter pylori could actually survive, and thrive, in the lining of the stomach as well as the upper duodenum... and more important, this tiny bacteria could be the "trigger" for an ulcer -- not stress, anxiety, low immune system or diet as once believed by the medical community.

After much ridicule from the scientific and medical community, both doctors perservered in proving their findings and have finally received the top award -- the Nobel Prize in Medicine.

Their work has stimulated research into microbes as possible reasons for other chronic inflammatory conditions, such as Crohn's disease, ulcerative colitis, rheumatoid arthritis and atherosclerosis, the Nobel assembly said in its citation.

What Is Helicobacter Pylori?

Here is some general information from the Helicobacter Foundation Website

Helicobacter pylori is a spiral shaped bacterium that lives in the stomach and duodenum (section of intestine just below stomach). It has a unique way of adapting in the harsh environment of the stomach.

The inside of the stomach is bathed in about half a gallon of gastric juice every day. Gastric juice is composed of digestive enzymes and concentrated hydrochloric acid, which can readily tear apart the toughest food or microorganism. Bacteria, viruses, and yesterdays steak dinner are all consumed in this deadly bath of chemicals. It used to be thought that the stomach contained no bacteria and was actually sterile, but Helicobacter pylori changed that.

The stomach is protected from its own gastric juice by a thick layer of mucus that covers the stomach lining. Helicobacter pylori takes advantage of this protection by living in the mucus lining.

Urea hydrolysis: urea is broken down to ammonia and carbon dioxide

Once H. pylori is safely ensconced in the mucus, it is able to fight the stomach acid that does reach it with an enzyme it possesses called urease. Urease converts urea, of which there is an abundant supply in the stomach (from saliva and gastric juices), into bicarbonate and ammonia, which are strong bases. This creates a cloud of acid neutralizing chemicals around the H. pylori, protecting it from the acid in the stomach. The reaction of urea hydrolysis is important for diagnosis of H.pylori by the breath test.

Gram stain of H. Pylori

Another defense H. pylori has is that the body's natural defenses cannot reach the bacterium in the mucus lining of the stomach. The immune system will respond to an H. pylori infection by sending white cells, killer T cells, and other infection fighting agents. However, these potential H. pylori eradicators cannot reach the infection, because they cannot easily get through stomach lining. They do not go away either, though, and the immune response grows and grows. Polymorphs die, and spill their destructive compounds (superoxide radicals) on stomach lining cells. Extra nutrients are sent to reinforce the white cells, and the H. pylori can feed on this. within a few days, gastritis and perhaps eventually a peptic ulcer results. It may not be H. pylori itself which causes peptic ulcer, but the inflammation of the stomach lining; i.e. the response to H. pylori.

H. Pylori causing a neutrophil reaction (active chronic gastritis) in the lining (mucosa) of the stomach

H. pylori is believed to be transmitted orally. Many researchers think that H, pylori is transmitted orally by means of fecal matter through the ingestion of waste tainted food or water. In addition, it is possible that H. pylori could be transmitted from the stomach to the mouth through gastro-esophagal reflux (in which a small amount of the stomach's contents is involuntarily forced up the esophagus) or belching, common symptoms of gastritis. The bacterium could then be transmitted through oral contact.