Bacteria as trigger for chronic gastrointestinal disorders.

Apart from acute infections, microorganisms may also induce or perpetuate chronic inflammatory diseases and reversible or irreversible proliferation of various cells in the gastrointestinal tract (the extreme being adenocarcinoma and lymphoma). Helicobacter pylori is not only involved in the pathogenesis of lymphoma and gastric adenocarcinoma. The steps and mechanisms of the carcinogenic process involve host predisposition, environmental factors, and strain virulence. The steps of lymphoma genesis include chronic inflammation, acquisition of mucosa-associated lymphoid tissue in the stomach, proliferation of the B lymphocytes in an inflammatory context, acquisition of genetic anomalies and dysregulation of the NF-κB pathway. The role of Campylobacter jejuni in immunoproliferative small bowel disease has also been shown and eradication of this bacterium can cure the lymphoma at its early stage. The evidence for the role of some bacteria in colon cancer development is discussed. Opportunistic pathogens are detected in the stools or mucosa of a proportion of subjects with Crohn's disease. They include Mycobacterium avium paratuberculosis, adherent invasive Escherichia coli, and Clostridium difficile. A dysbiosis has been repeatedly observed in patients with inflammatory bowel disease. Instability of the dominant microbiota and decreased biodiversity (especially in the firmicutes phylum) are major characteristics. The decrease of Faecalibacterium prausnitzii seems to have a prognostic value to predict relapse of Crohn's disease after surgery. Finally, important perspectives are opened by new tools such as metagenomics and metabolomics of the gastrointestinal ecosystems. Major tracks concern irritable bowel syndrome, colon cancer and obesity.