However, the results of such studies are not conclusive, and theory of infectious aetiology of Crohn’s disease

has never been proved. A major problem in identification of possible infectious causative factor of Crohn’s disease comes from the fact that studies performed so far, including those which utilized bacterial 16S rRNA detection, were generally focused on terminal ileum and colon,16 which represent sites most commonly affected with Crohn’s disease, and ileum-related lymphatic follicles and nodes.14,17 Since terminal ileum both in healthy people and in Crohn’s disease patients is an area of high bacterial density #third keyword# and contains enormous number of different bacterial strains, it is hard to distinguish whether Inhibitors,research,lifescience,medical any isolated bacteria represents a pathogen, a saprophyte, or it is the case of superinfection. We propose a different approach for isolation of bacteria, which may cause

Crohn’s disease. The approach include identification of such bacteria in inflamed gastric mucosa in patients who suffer from Crohn’s gastritis. Crohn’s gastritis is an uncommon form of Crohn’s disease. Although it is estimated that symptomatic involvement of upper gastrointestinal tract is present in less than 4% of patients, who suffer from Crohn’s disease,18 histological changes Inhibitors,research,lifescience,medical of gastric mucosa, including those consistent with gastric Crohn’s disease may be present in more than 40% of patients with the disease.19,20 Contrary to terminal ileum, human stomach is a place where very limited number of bacteria may survive, so that finding of a bacteria other than Helicobacter Inhibitors,research,lifescience,medical pylori in gastric mucosa of patients with gastric Crohn’s disease may point that such bacteria is a pathogen. The detection of 16S bacterial rRNA by PCR represents a convenient method for identification of bacteria. This gene is present in bacteria and has remained conserved during evolution. The method has furthermore proved its usefulness in the discovery of another intestinal pathogen, Trophyrema Whipplei in 1992,21 as well as identification of new Helicobacter species.22 Therefore, with utilization of this method Inhibitors,research,lifescience,medical may identify bacteria responsible

for appearance of Crohn’s disease, providing that they are still present in gastric mucosa at the time of the study. We believe that it would be best to take gastric biopsies from two groups of people, Anacetrapib who did not receive any prior therapy with proton pump inhibitors, since such therapy may result in decreased gastric acid secretion and gastric bacterial colonization which might adversely affect the results of the study. One group would consist of patients who have clinical signs of gastric involvement with Crohn’s disease with appropriate symptoms such as upper abdominal pain, vomiting and nausea and consistent endoscopic findings and who are not infected with H. pylori. The other group would include Crohn’s disease patients who have no clinical symptoms attributable to gastric Crohn’s disease and no H.