Chronic inflammatory bowel diseases (IBDs), like Crohn’s disease and ulcerative colitis, are correlated with an imbalance in the microbiota.
The prevalence of IBDs is 1 case per 1,000 inhabitants in Western Europe1 . They have a profound effect on quality of life. Clinical symptoms and signs can vary (diarrhea that can be hemorrhagic, abdominal pain). Their course is unpredictable, marked by alternating periods of flares and remissions2 .
In Crohn’s disease (CD), inflammation in the intestinal mucosa progressively develops into stenosis and fistulas and/or abscesses. In ulcerative colitis (UC), the inflammatory lesions are typically more superficial and less harmful. Chronic inflammation can cause irreversible anatomic damage and promote the onset of gastrointestinal cancers.
The pathophysiology of IBDs
The onset of IBDs results from a genetic predisposition, environmental factors, the immune system, and the intestinal microbiota. Studies in twins have demonstrated the involvement of genetic and environmental factors3.
Involvement of the microbiota
Current microbiota research suggests the existence of an imbalance between “anti-inflammatory” and “pro-inflammatory” bacteria in patients with IBDs. This dysbiosis seems to be related to a predominance of pro-inflammatory bacteria (Enterobacteria, Fusobacteria), the presence of adhering Escherichia coli, and the scarcity of anti-inflammatory bacteria belonging to the genus Firmicutes (Clostridia, Faecalibacterium)4.
In particular, dysbiosis generated by the loss of Faecalibacterium prausnitzii can have a pro-inflammatory effect4.This dysbiosis may cause inflammation in two ways, which are not mutually exclusive: either directly, through the production of pro-inflammatory microbial molecules, or indirectly by modifying structural elements in the intestinal ecosystem5.
The goal of treatment is to reduce symptoms, but also to reduce the risk of irreversible anatomic damage and cancers caused by chronic inflammation. Corticosteroid therapy, immunomodulators, and, increasingly frequently, TNF inhibitors remain the standard treatments for IBDs. Some probiotics have also shown moderate effectiveness in some cases to treat IBDs6.
1. Cosnes J et al. Epidemiology and natural history oj inflammatory bowel diseases. Gastroenterology 2011 ; 140 : 1785-94. http://www.gastrojournal.org/article/S0016-5085(11)00164-8/abstract?referrer=https%3A%2F%2Fwww.ncbi.nlm.nih.gov%2F
2. Inserm.fr, microbiote intestinal et santé, http://www.inserm.fr/thematiques/physiopathologie-metabolisme-nutrition/dossiers-d-information/microbiote-intestinal-et-sante
3. Halfvarson J, Bodin L, Tysk C, Lindberg E, Jarnerot G. Inflammatory bowel disease in a Swedish twin cohort: a long-term follow-up of concordance and clinical characteristics. Gastroenterology 2003 ; 124 : 1767-73. https://www.ncbi.nlm.nih.gov/pubmed/12806610
4. Sokol H, Seksik P, Furet JP, et al. Low counts of Faecalibacterium prausnitzii in colitis microbiota. Inflamm Bowel Dis 2009 ; 15 : 1183-9.
5. Quevrain E, Maubert MA, Michon C, et al. Identification of an anti-inflammatory protein from Faecalibacterium prausnitzii, a commensal bacterium deficient in Crohn’s disease. Gut 2016 ; 65 : 415-25.
6. Kostic AD, Xavier RJ, Gevers D. The microbiome in inflammatory bowel disease: current status and the future ahead. Gastroenterology 2014 ; 146 : 1489-99.