Patchy distribution of mucosal lesions in ileal Crohn's disease is not linked to differences in the dominant mucosa-associated bacteria: a study using fluorescence in situ hybridization and temporal temperature gradient gel electrophoresis.

BACKGROUND: The mucosa-associated bacteria (MAB) are suspected of being involved in the pathogenesis of Crohn's disease. We analyzed and compared the MAB in noninflamed and inflamed ileal mucosa of Crohn's disease patients (n = 22). METHODS: Tissue samples from the inflamed ileal mucosa and from the adjacent noninflamed ileal mucosa were taken from surgical resection specimens. The MAB were investigated using fluorescence in situ hybridization with 7 group-specific probes and temporal temperature gradient gel electrophoresis (TTGE). RESULTS: Samples from both noninflamed and inflamed mucosa were obtained from 15 patients. The distribution of the bacterial populations was not different between noninflamed and inflamed mucosa. The Bacteroidetes phylum was dominant and accounted for 29% of MAB (0%-74%) in noninflamed tissues and 32% (0%-70%) in inflamed areas. The gamma Proteobacteria represented 12% (0%-70%) of MAB both in noninflamed and inflamed areas. The Clostridium coccoides group (Firmicutes phylum) represented 15% of MAB in noninflamed tissues versus 7% in inflamed areas. For most of the patients the similarity index between TTGE paired profiles was very high. CONCLUSION: The dominant MAB do not differ between noninflamed and inflamed ileal mucosa in Crohn's disease. This argues against a localized dysbiosis to explain the patchy distribution of mucosal lesions.

[Epidemiology and risk factors of inflammatory bowel diseases]. / Epidémiologie et facteurs de risque des maladies inflammatoires chroniques de l'intestin.

Inflammatory bowel diseases (IBD) are a public health problem in developed countries as 1 per 1000 people suffers from these diseases. Most of affected people are young adults. The incidence of IBD has increased considerably in western countries since the Second World War and it is beginning to level off. On the other hand, incidence is still rising in low incidence areas such as Eastern Europe, Asia and developing countries. Differences in incidence across age, time, and geographic areas suggest that environmental factors are acting in IBD but so far cigarette smoking and appendectomy are the only risk factors which have been consistently demonstrated. An important role for genetic factors in IBD was first suggested by epidemiological studies showing familial aggregation of IBD and by twin studies. In 2001, the first CD susceptibility gene, NOD2/CARD15 on chromosome 16, has been characterized. Other susceptibility genes have been localized. Their identification should help to understand the complex interaction between the environment and the intestinal immune system from which IBD are originating.

Relevance of serologic studies in inflammatory bowel disease.

The serologic panel for inflammatory bowel disease (IBD) is rapidly expanding. Antineutrophil cytoplasmic antibodies (ANCA) and anti-Saccharomyces cerevisiae mannan antibodies (ASCA) have remained the most widely studied markers, but immune reactivity against a new group of bacterial antigens such as I2, OmpC (outer membrane porin C), and flagellin, has been described in Crohn's disease. Several clinical avenues have been explored, such as the usefulness of serologic markers as screening tools for IBD and in accelerating a diagnosis in patients with indeterminate colitis. Another area of interest is disease stratification. Emerging data suggest there is a diversity of qualitative and quantitative responses to environmental antigens that differs among groups of IBD patients and may be associated with different clinical behaviors. As a result, it may be possible to tailor therapy on the basis of serologic responses. Prospective studies are needed before translating this concept into clinical practice. Clustering of IBD patients into more homogeneous subgroups based on antibody responses may help to unravel the pathophysiology of subsets of IBD.