Nowadays, Crohn’s disease exact causes are unknown. It is thought that it occurs when a person’s immune system attacks healthy tissues of the digestive tract, producing inflammation. Nevertheless, recent studies show that it may be caused by a disbalance between commensal bacteria and pathogenic bacteria of the intestinal microbiota (dysbiosis) in genetically predisposed patients.
Crohn's disease is characterized by being an inflammatory bowel disease. This means that when a patient has Crohn's disease, he or she will experience an inflammation on their digestive tract which leads to abdominal pain. It can affect any part of the intestinal tract from the mouth to the anus, but it normally affects the ileum, colon and rectum.
Recent discoveries seem to suggest that this disease could have a bacterial origin. Studies have shown that there was an increase or decrease of certain bacteria in patients with Crohn’s disease’ intestinal microbiota that healthy people did not have.
Patients with this disease appear to have a genetic predisposition that prevents them from efficiently recognizing and eliminating pathogenic bacteria, leading to the uncontrolled proliferation of harmful bacteria and a decrease of helpful bacteria. More specifically, they have smaller density of Faecalibacterium prausnitzii (which has antiinflammatory properties) and an excess of Proteobacteria.
Urease is a virulence factor found in various pathogenic bacteria, which, due to its enzymatic activity, can have a toxic effect on human cells. But how does bacterial Urease play a role in the inflammation of our own digestive track? Bacterial urease allows the intestinal microbiota to use the host’s nitrogen supplies as a substrate for bacterial production of amino acids. Thus, it promotes dysbiosis.
To further understand the role played by bacterial Urease in Crohn's disease researchers are specifically looking into the high concentrations of amino acids detected in the feces of patients with the disease. This occurs due to the supply of significant amounts of nitrogen for amino acid synthesis and, therefore, the involvement of bacterial urease that transforms urea into ammonia. Researchers confirmed in a study of 90 patients that were under 22 years of age with Crohn's disease that there was a correlation between high fecal amino acid concentrations and calprotectin concentrations and, therefore, the severity of disease.
In addition, an investigation in which mice, which had previously undergone an intestinal wash with antibiotics, were administered E. coli Ure- or E. coli + showed that the Ure- strain promoted a bacterial recolonization while the positive strain leads to a dysbiosis. The positive strain was also administered to mice who already had inflammatory bowel disease and the already existing symptoms increased. These studies confirm that Urease activity is intrinsically related with Crohn’s disease and therefore, it could be a possible therapeutic target.
By Yaiza Anido Figueirido and Iara Inés Méndez Grande. Group 03 of Microbiology. 2nd year of Biotechnology Degree.
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