PAVLOV'S COLI

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Inflammatory Bowel Disease

Inflammatory bowel disease (IBD) describes the chronic inflammations of parts of the intestine and is a collective of several further specified illnesses. The most common conditions are ulcerative colitis and Crohn's disease. It is classified as an autoimmune disease for which no cure has been developed. Current treatments include immunosuppression, surgery, antibiotics and nutritional therapies. This disease is a severe burden for the patients as well as it causes increasing direct (treatment) and indirect (absenteeism from work) costs for society. Furthermore, only in Europe 2.5 million people are affected by IBD and the number of cases is increasing world-wide¹.
Unfortunately there are no characteristic blood markers to distinguish the different forms of IBD. The diagnosis relies mostly on the location of inflammation observed during a colonoscopy. Also the underlying trigger of the disease is not completely understood but correlation studies proposed factors such as diet, genetic predisposition, breach of the intestinal barrier and unfavorable alteration of the microbiota, called dysbiosis². The diversity of the microbiota is noticeably reduced^2,2 in IBD patients and the composition of the gut flora changes from symbiotic to predominantly pathobiotic microbes¹.
The inflammation of the intestine partially interrupts the integrity of the layer of epithelial cells lining the intestine. This cell layer separates the gut lumen containing trillions of microbes from the body. The damage to this essential barrier compromises the selectivity and allows for penetration of immunogenic antigens from the lumen across the epithelial layer^1, which enhances the inflammation reaction.

References:

[1] Maciej Chichlowski and Laura P Hale. “Bacterial-mucosal interactions in inﬂammatory bowel disease: an alliance gone bad”. In: American Journal of Physiology-Gastrointestinal and Liver Physiology 295.6 (2008), G1139–G1149.

Team:ETH Zurich/Description