Inflammatory Bowel Disease (IBD)

Inflammatory Bowel Disease (IBD) is a general term that covers several conditions in which the intestine is persistently inflamed. The two main forms of IBD are Crohn's Disease and Ulcerative Colitis (UC). IBD should not be confused with IBS (Irritable Bowel Syndrome), a completely separate condition in which the intestine is not damaged.

Crohn's and UC are long-term conditions that, although mostly starting in young adults, can start at any age. The main symptoms are diarrhoea and pain and blood in the stool. Currently, there is no cure. Treatments include a range of drugs that reduce the inflammation and, in severe cases, surgery to remove the damaged intestine.

There are three main factors thought to be responsible for intestinal inflammation associated with IBD; genetics, the immune system and gut microflora. It has only recently become clear that these diseases centre on the immune cells and tissues in the intestine reacting incorrectly to the normal gut microflora.

In human studies, an imbalance in colonic bacteria has been described, including a reduction in potentially protective organisms such as Bifidobacteria spp. and Lactobacilli spp. An increase in pathogenic organisms such as Escherichia coli was also seen which, along with inflammation of the intestinal mucosa, results in the development of lesions on the gut wall (1).

The theory put forward to explain bacterial involvement in IBD is as follows; “a pathogen, possibly a bacterium, reaches the intestine in large numbers and triggers the immune system but, instead of stopping when the pathogen has been defeated, the inflammation carries on as though there were dangerous invaders still present(2).” It is thought that this inflammation continues due to the immune system reacting mistakenly to the normal gut microflora.

The initial trigger for the inflammation is when a pathogen passes through the gut mucosa of the intestinal wall. In normal subjects the epithelial cells form tight junctions and only allow small nutrient particles of digested food through. Patients with IBD have increased gut permeability (‘leaky gut’), which may also allow bacteria to pass through the gut wall.

It is thought that if the introduction of beneficial bacteria, in the form of probiotics, can change the types of bacteria in the gut, then they may be able to alter the immune response of the gut to its microflora. In other words, if you increase the number of beneficial bacteria and reduce the number of pathogenic bacteria, then the immune system may react in the correct way and not cause continual inflammation. Treatment with probiotics has been shown to reduce intestinal inflammation and inflammatory response in experimental models of colitis and to reduce symptoms and inflammation in patients with IBD (3).

The evidence suggests that increasing the number of beneficial bacteria in the small intestine and colon may improve the health of patients suffering from IBD. The result can include a reduction in the severity of symptoms, longer remission periods and improved immune function. Patients may also be able to reduce their prescribed medication and even delay, or prevent, the need for surgery.

References
1. Guarner F. (2003), “Microecology as a target for therapeutic intervention in inflammatory bowel disease”, IDrugs, 6(9):868-73.
2. Cartwright P. 2003), Probiotics for Crohn’s and Colitis, Prentice Publishing.
3. Penja J.A., Rogers A.B., Ge Z., Ng V., Li S.Y., Fox J.G., Versalovic J. (2005), “Probiotic Lactobacillus spp. diminish Helicobacter hepaticus-induced inflammatory bowel disease in Interleukin–10 deficient mice”, Infect Immun. Feb, 73(2): 912:20.