Inflammatory bowel diseases (IBD) are chronic, inflammatory conditions of the gastrointestinal tract and consist of Crohn’s disease (CD) and ulcerative colitis (UC). IBD has the highest incidence in teenagers and young adult, and diarrhea and abdominal pain significantly impacts on quality of life. The cause of these diseases is uncertain and therefore there is no cure for either CD or UC. IBD is thought to arise from an aberrant immune response in genetically susceptible individuals. Current therapies attempt to improve symptoms by modulating the immune system but research now focuses on what might be driving this immune response and the most likely candidate is the gut microbiome. Preclinical studies, in collaboration with scientists in France (Langella P, INRA Paris), are elucidating the roles and therapeutic potential of commensal bacteria in models of IBD. A 2015 study by Natividad J et al found that selected bacterial groups, involved in gut health, are important for protecting the colon against injury and inflammation in mouse models colonized with gut bacteria from UC patients and healthy controls. A recent study from the Farncombe Family Digestive Health Research Institute (Moayyedi P et al. Gastroenterology 2015) assessed how modulating gut bacteria with fecal microbiota therapy (FMT) can induce remission in patients with active UC in the first randomized trial in this area. It is an example of the Institute’s ability to translate promising results of preclinical studies into patients. Psychiatric co-morbidity is common in chronic GI diseases including IBD an reflects the intimate relationship between the gut and brain. Previous preclinical studies in the Institute has shown that gut inflammation alters brain function and behaviour (Bercik P Gastroenterology 2010) and can be attenuated with selected probiotics (Bercik P 2011). More recently that group has shown that in a preclinical model of early stress that results in persistent changes in behaviour, the expression of depression was dependent on the presence of gut bacteria (De Palma G et al Nat Commun 2015).
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