Helicobacter pylori is a bacterium that can colonize the human gastric mucosa causing gastritis, ulcers and in some cases the onset of stomach cancer. E 'was discovered the mechanism after which H. pylori inactivates a protein whose function is suppression of tumor growth in host cells.
The stomach is a hollow muscular structure that is localized between the esophagus and intestines. Its task is to complete the demolition of the fragments of food from bite to break down the chemical bonds of molecules present in food, through the action of acids and enzymes digestive secretions from gastric glands. This
degradative action of the stomach is designed to provide absorption molecules and nutrients in the small intestine.
The inner surface of the gastric mucosa is raised in large folds following all the internal morphology of the organ.
These folds allow both the expansion of the organ during the meals that the physiological transport of liquids along the main street towards gastric intestine.
HELICOBACTER PYLORI
Helicobacter pylori bacterium is a spiral, Gram-negative, which can colonize the human gastric mucosa. More than 50% of the population worldwide is H. pylori. The infection is often asymptomatic but in 10-20% of cases it can cause gastritis and ulcers, particularly in the duodenum, the first part of the intestine. The
gastritis is a chronic inflammation of the stomach, while the ' ulcer is a lesion of the mucosa, which produces burning or intense pain, especially on an empty stomach. Sometimes ulcers can bleed and eventually cause anemia.
The long-term infection with H. pylori is associated with an increased (2-6 times) risk of developing a lymphoma MALT , a cancer of lymphoid tissue in mucous membranes, especially of developing gastric cancer .
Gastric cancer is the second most common cancer in the world , particularly in countries like China or Colombia where infection H. pylori affects more than half the child population.
man is currently the only known reservoir of infection for this bacterium, which most likely mode of transmission is oral and fecal-oral route. Another possible route of infection could be through contact with contaminated water.
DIAGNOSIS AND TREATMENT
The procedure of choice for diagnosing infection H. pylori is represented by during digestive endoscopy biopsy, the histological examination, the test of urea hydrolysis and microbial culture.
less sensitive tests are those of a serological and breath.
Once the presence of the bacterium, an attempt to eradicate the infection through the use of a triple therapy with antibiotics and specific drugs inhibiting gastric acid secretion.
As you develop stomach cancer are known
different strains of H. pylori, some of which have been completely sequenced within their genome. More 1500 genes were identified, one third of which are considered the basis of the pathogenic mechanisms of infection.
capacity H. pylori to cause disease is closely linked to a protein called CagA his . This molecule is highly virulent, is able to cause local inflammation by stimulating abnormal cell growth and division which can then lead to the onset of cancer.
A group of researchers has recently characterized the specific pathogenic mechanism mediated by the protein CagA. Target of this molecule was found to be a bacterial molecule, synthesized in the human gastric cells, whose physiological function suppression of tumor growth.
H. pylori injects CagA protein in epithelial cells lining the stomach . Here, CagA is able to interfere with their different mechanisms of gastric cells, destroying a number of important functions. Among the targets of CagA is RUNX3, a protein known to be an important tumor suppressor stomach , whose reduction is closely associated with the development of this disease. RUNX3 protein is in fact a transcription factor, can modulate the expression of genes that control growth and cell death.
For the first time was identified a domain within the amino acid sequence of CagA protein can bind a specific region of RUNX3 : as a result of this interaction, the RUNX3 protein undergoes degradation, resulting in failure of the tumor suppressor role within the cell.
This study outlined a particular mechanism for the genesis of stomach cancer induced by H. pylori. The researchers propose in the future to synthesize new molecules that can specifically inhibit the interaction between CagA and RUNX3, blocking its degradation and thus could prevent the serious complications caused by H. pylori in the stomach.
(by Roberto Insolia - Press-Stampa.net)
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