מתוך medicontext.co.il
By Karla Gale
NEW YORK (Reuters Health) – The mucosal surface of the bowel in healthy subjects is nearly sterile, German investigators report in the January issue of Gastroenterology. However, in patients with persistent colitis, the bacterial burden of the mucosa increases with the severity of disease.
Researchers obtained biopsies from the ileum and colon of 40 asymptomatic control subjects, 28 patients with colitis that resolved within 2 months, and 104 patients with indeterminate colitis. Biopsies were also retrieved from 119 patients with ulcerative colitis and 54 with Crohn's disease.
Dr. Alexander Swidsinski, of Charite Humboldt Universitat in Berlin, and colleagues gently washed the specimens in physiologic saline and then subjected them to hypotonic lysis. Culture of the lysate showed that the concentration of mucosal bacteria increased progressively, from self-limiting and indeterminate types of colitis to ulcerative colitis. Concentrations were highest in those with Crohn's disease. Bacterial species did not differ significantly between groups.
A thick bacterial film was observed when microbial concentrations exceeded 10,000 colony forming units/µL. Electron microscopy revealed bacteria in cells close to the basal lamina, rather than in superficial epithelium cells. Adjacent cells had a normal appearance.
"Surprisingly, concentrations of mucosal bacteria were higher in non-inflamed than inflamed mucosa," the investigators write.
The ability to prevent fecal bacteria from closely contacting the epithelial surface is disturbed in patients with IBD primarily due to local inflammatory changes, the researchers conclude. The findings suggest a specific host response, "resulting from peculiarities of immunity, genetic disposition, or symbioses-like interactions," rather than a specific pathogen being responsible.
Dr. Jonathan Braun, of the University of California Los Angeles School of Medicine, suggests in an editorial that the inflammatory disorder appears to enhance bacterial-epithelial adhesion. These could be due to a mucosal disorder "such as impaired host attenuation processes or aberrant epithelial glycan expression," he writes.
Dr. Braun, in an interview with Reuters Health, theorized that bacterial concentrations are lower over areas of inflammation because those epithelia have been sloughed off, resulting in fewer binding sites for bacteria.
Overall, however, "people with this disease may be colonized with bacteria that are better at binding to and invading epithelial surfaces," he said. "Another idea is that structures onto which bacteria bind may be more highly expressed in people with these diseases."
The implication, he added, is that more microbial binding puts individuals at risk for the disease.
Dr. Braun said the new findings demonstrate "a greater need for understanding the details of bacterial biology in the gut and a level of interaction between the gut bacteria and the lining of the intestine that we previously hadn't appreciated."
More detailed understanding will help clinicians assess and treat this category of intestinal diseases, he added.
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