Helicobacter pylori

                                  Helicobacter pylori

Cientists isolate the component of the bacterium that causes ulcers

Almost half the world's population is infected with the gastrointestinal tract bacteria Helicobacter pylori, a causative agent of gastritis, ulcers and stomach cancer. A Japanese research team has found the component of the bacterium that causes ulcers directly (a protein called cow), and also the stomach cells that serve as a gateway VacA (VacA receptor). The VacA protein can now be used to create a vaccine, and its natural receptor variants allow predict which people are most at risk.
The discovery in 1984 of the Helicobacter bacterium common in the human stomach, was a causative agent of gastritis, ulcers and stomach and duodenal cancer opened an unsuspected route of treatment (or prevention) of diseases that were thought to be associated with meals spicy and stress. Today we know that most ulcers can be cured with antibiotics combined two weeks of killing Helicobacter stomach colony.

But while half of people are infected with Helicobacter, only a small fraction develops ulcers, and stomach cancer alone. Scientists suspect that the discrepancy was due to natural variations in the virulence of some other strains of Helicobacter and, on the one hand and individual susceptibility to the disease on the other. The Japanese have found the most likely basis for both power range.
The study, published today in Nature Genetics, is a collaboration between the National Institute for Basic Biology in Okazaki, and the Universities of Kobe, Shinshu, Nagasaki and Tokyo. The results refer to mice, but the bacterium is the same in rodents and humans, and receiver mouse stomach cells exists in our species.
The attack of Helicobacter to gastric mucosa is executed by bacterial VacA protein. It binds to a specific receptor on the surface of the cells lining the stomach. VacA binding to its receptor activates a biochemical cascade that causes cells to become detached from the mucosa, inner fragile tissues exposing the corrosive action of gastric acid. So ulcer originates.

Why not all those infected develop ulcer? On the one hand, because Helicobacter is very diverse. The gene that makes the VacA protein (the gene vacA) exists in all strains, but is highly variable, and some strains are much more active VacA protein. It's a matter of luck which strain touch us. Significant that one of the most active variants of VacA (s2) is much more common in ulcer than those with only gastritis.
Variable genes
The other factor contributing to the discrepancy (between the many and the few infected ulcer) is the variability in certain human genes, and work identifies two strongest candidates. VacA receptor (called Ptprz) is not in the stomach cells to facilitate the attack of Helicobacter (evolution is blind, but not stupid). It is for detecting other human molecule (the pleiotropin) to finely modulate various aspects of the biology of the gastric mucosa.

Japanese scientists have found that pleiotropin administered in high amounts, can produce obvious signs of ulcer. Individuals, therefore, may differ in their susceptibility to attack of Helicobacter due to natural variability in the gene that produces the receptor VacA, or manufactured by the pleiotropin, or both. Of course, you can not rule out other sources of variability.
Gastroenterologist Richard Peek, of the School of Medicine at Vanderbilt University (Tennessee, USA), also points out today in Nature Genetics: "Understanding the role in the origin of the ulcer of the determinants of the virulence of Helicobacter pylori can contribute the development of a vaccine. " One obvious possibility is to generate antibodies against cow. Peek added that the finding VacA receptor "can allow the identification of infected individuals increased risk of disease." Helicobacter Since many tumors also causes stomach, it may be one of the first cases where a cancer is reached prevent some doses of antibiotics. The discovery that stomach ulcers and gastritis caused them a lot of bacteria, Helicobacter pylori, not only won them a Nobel (and infection) with their authors, Barry J. Marshall and J. Robin Warren. Also completely it changed the way to treat the disease: surgery and painkillers to combinations of antibiotics. In the case of an infection, the next step is to find a vaccine. And it is the Chinese team has published their findings in The Lancet, with promising efficacy of currently 72%.

The trial is a classic exercise of comparison between vaccinated and unvaccinated people (the control group) in which no one knows who is getting the drug and who is not, which is avoided or equals the placebo effect. This form of testing is called double-blind because no one, neither the volunteers nor the health to serve them know why you are taking each.
For work to 4,464 boys were selected 6 to 15 years in the province of Jiangsu, of which 4,403 were under control three years later. They were chosen to ensure that young people had not been in contact with the bacteria. With these two groups, one receiving the vaccine and another that took (the vaccine is oral) placebo were formed.
The result is that, in all, 64 cases were recorded helicobacter infection. Of these, 50 were in the group that did not take the drug, and the remaining 14 in the of those who are actually vaccinated. Taking the raw numbers, this represents a reduction of cases (protection rate) of 72%. When data is adjusted and the time variable in the trial were all introduced, low efficiency slightly, to 71.8%.

Less than 1% of the participants in the two groups (12 in total, of which five had been vaccinated) had to leave for health reasons, but the authors rule out adverse effects were related to immunization.
The trial authors themselves admit that the time has passed (three years) is not enough, and we have to wait to confirm or exclude that the protective effect of the drug is maintained, but indicate a breakthrough for protecting people of this disease. The beneficiaries are potentially hundreds of millions: it is estimated that between 5% and 15% of the population has complications from a gastric ulcer at least once in your life

References:

Javier Sampedro.

 Nature Journal

@RdzgCarlos

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