HOW DO HOST MICROBE INTERACTIONS IN THE GI TRACT MAINTAIN HEALTH?
GI tract communities and their interaction with the immune system can play roles in intestinal epithelial development and activity, education of the immune system, integrity of the mucosal barrier, and even contribute to drug metabolics1.
Commensal bacteria can aid host immunity by preventing the successful colonization and invasion by harmful bacteria.
If there is a defect in the immune system or in the mucosal barrier, the host can be vulnerable to bacterial infection and activation of the immune system1
WHAT IS INTESTINAL DYSBIOSIS?
Over 99% of bacteria in the gut can be classified into four major divisions: Firmicutes, Bacteroidetes, Proteobacteria and Actinobacteria2. This diverse community of commensal gut bacteria metabolizes nonabsorbable dietary carbohydrates, exfoliated epithelial cells and mucus-producing metabolites that influence the function of intestinal epithelium, energy balance of the host and immune response3. Gut microbes are also supported by a nutrient rich environment provided by the host. In turn, these bacteria produce short chain fatty acids (SCFA) (such as butyrate and acetate) that protect the gut by acting as anti-inflammatories.
Dysbiosis is simply an imbalance in these microorganisms, and can lead to reduction of the protective fatty acids and thus promote a pathological, inflammatory state. As a result, it can play a role in autoimmune diseases, colon cancer, and allergies, just to name a few.
WHAT SPECIFIC DYSBIOSIS EXISTS IN IBD?
Inflammatory bowel disease patients have shown a markedly different shift in the composition of bacteria in comparison to a normal healthy gut, a state known as dysbiosis, as explained above. Microbial numbers are often depressed in IBD demonstrating a decrease in bacterial biodiversity.
In both ulcerative colitis and Crohn’s disease, Firmicutes and Bacteroides are decreased, whereas Actinobacteria and Proteobacteria are increased4. Studies have demonstrated that the gut-protecting bacterium that is significantly decreased in ulcerative colitis and Crohn's disease is the Lachnospiraceae bacterium Faecalibacterium prausnitzii. An increase in adherent-invasive Escherichia coli (AIEC), a gut-injurious organism, is also found in Crohn's disease5.
TO WHAT EXTENT DOES DIET AFFECT THE MICROBIOTA?
There has not been much evidence that differing diets in different human populations results in vastly different microbiota. However, De Fillippo C, et al were able to show that the fecal microbiota of European children is significantly different than that of Burkina Faso, a village with a high fiber diet. BF children had:
- More Bacteroidetes, but less Firumicutes bacteria
- Less Enterobacteriaceae (pro-inflammatory)
- Significantly more short-chain fatty acids, known to protect against inflammation.
In addition, it has been shown that exposure to a western diet composition results in decreased microbial diversity in rats, as measured by the Shannon-wiener diversity index.
WHAT ARE PRE- AND PRO-BIOTICS?
Probiotics – ingested microorganisms or bacteria that are believed to be associated with benefits for humans and animals. They can be found in foods such as yogurt 6.
Prebiotics – nondigestible carbohydrates that potentially stimulate growth of healthy probiotic bacteria. Found in whole grains, bananas, onions, garlic, honey artichokes, etc.6
PROBIOTIC TREATMENT OF IBD
An increasing number of studies have been completed with probiotics and IBD. Improvement in ulcerative colitis and pouchitis has been seen with VSL3 a high potency probiotic “cocktail”, containing probiotic lactic acid bacteria and bifidobacteria (8 different types) 7, and with E.coli Nissle 1917, a proven probiotic bacterial strain8,9,10. There is little evidence for probiotic treatment of Crohn’s disease, but it has been found to have decreased clinical and endoscopic recurrence post-operatively with the addition of VSL311.
PREBIOTIC TREATMENT OF IBD
Over the recent decade, there have been limited studies done on the role of prebiotics in IBD. However, some evidence based treatments have been clinically proven on the induction and remission of IBD. Improvement in ulcerative colitis, pouchitis and Crohn's disease has been seen in prebiotic FOS/Inulin combination therapy12,13,14
For example, in one experiment, HLA-B27 transgenic rats were genetically modified to develop spontaneous colitis. When fed with long chain inulin type fructans and short chain oligofructose (prebiotics), colitis was reduced as measured by decreased GCS and inflammatory histologic scores. The conclusions of the study showed increased Lactobacillus and bifidobacterium (probiotics) in the gut, decreased tissue proinflammatory cytokines, and increased immunomodulatory molecules.
WHAT DOES THE FUTURE OF DIETARY INTERVENTION IN IBD LOOK LIKE?
Future use of alternative therapies such as probiotics and prebiotics can lead to the reduction and replacement of pharmaceutical therapies and even surgery. Dietary therapies in IBD are novel and increasingly investigated in studies over the last two decades. However, well-powered, randomized controlled trials that study different probiotic strains, doses and administration routes and prebiotic fibres are required in order to further research in this field. The microbiota of the gut and its interaction with probiotics and prebiotics also requires more insight in order to benefit research into the complex disorder of inflammatory bowel disease.
REFERENCES
1. Institute of Medicine (US) Forum on Microbial Threats. Ending the War Metaphor: The Changing Agenda for Unraveling the Host-Microbe Relationship: Workshop Summary. Washington (DC): National Academies Press (US); 2006. 6, Manipulating Host-Microbe Interactions: Probiotic Research and Regulations. Available from: http://www.ncbi.nlm.nih.gov/books/NBK57065/
2. Di Gioia, D. (2011). Introduction to Intestinal Microbiota (n.d.) Retrieved February 10, 2016 from http://www.mf.uni-mb.si/mf/instituti/IPweb/html/DiGioiaD%20Introd uction%20to%20intestinal%20microbiota.pdf
3. Sartor, R. B., & Mazmanian, S. K. (2012). Intestinal Microbes in Inflammatory Bowel Diseases. The American Journal of Gastroenterology Supplements, 1(1), 15–21. http://doi.org/10.1038/ajgsup.2012.4
4. Sasaki, M., & Klapproth, J.-M. a. (2012). The Role of Bacteria in the Pathogenesis of Ulcerative Colitis. Journal of Signal Transduction, 2012(Cd), 1–6. http://doi.org/10.1155/2012/704953
5. Carrière, J., Bretin, A., Darfeuille-michaud, A., & Barnich, N. (2015). Exosomes Released from Cells Infected with Crohn’s Disease – associated Adherent-Invasive Escherichia coli Activate Host Innate Immune Responses and Enhance Bacterial, 0(0),1–13.
http://doi.org/10.1097/MIB.0000000000000635
6. Zeratsky, K. (n.d.). Consumer health: Do I need to include probiotics and prebiotics in my diet? Retrieved May 18, 2016, from http://www.mayoclinic.org/healthy-lifestyle/consumer-health/expert-answers/probiotics/faq-20058065
7. Miele E, Pascarella F, Giannetti E et al. (2009). Effective of a probiotics preparation (VSL#3) on induction and maintenance of remission in children with ulcerative colitis. Am J Gastroenterol, 104: 437-443.
8. Kruis W, Schutz E, Fric P, et al. (1997). Double-blind comparison of an oral Escherichia coli preparation and mesalazine in maintaining remission of ulcerative colitis. Aliment Pharmacol Ther, 11: 853-858.
9. Rembacken BJ, Snelling AM, Hawkey PM et al. (1999). Non-pathogenic Escherichia coli versus mesalazine for the treatment of ulcerative colitis: a randomized trial. Lancet, 354: 635-639.
10. Kruis W, Fric P, Pokrotnieks J et al. (2004). Maintaining remission of ulcerative colitis with the probiotic Escherichia coli Nissle 1917 is as effective as with standard mesalazine. Gut, 53: 1617-1623.
11. Fedorak RN, Feagan BG, Hotte N, Leddin D, Dieleman LA, Petrunia DM, et al. (2015). The probiotic VSL#3 has anti-inflammatory effects and could reduce endoscopic recurrence after surgery for Crohn's disease. Clin Gastroenterol Hepatol,13(5): 928-935.
12. Hanai H, Kanauchi O, Mitsuyama K et al. (2004). Germinated barley foodstuff prolongs remission in patients with ulcerative colitis. Int J Mol Med, 13: 643-647.
13. Welters CF, Heineman E, Thunnissen FB et al. (2002). Effect of dietary inulin supplementation of inflammation of pouch mucosa with an ileal pouch-anal anastomosis. Dis Colon Rectum, 45: 621-627.
14. De Preter V, Joossens M, Ballet V et al. (2013). Metabolic profiling of the impact of oligofructose-enriched inulin in Crohn’s disease patients: a double-blind randomized controlled trial. Clin Transl Gastroenterol, 4(1): e30.
15. Bollinger, R. R., Barbas, A. S., Bush, E. L., Lin, S. S., & Parker, W. (2007). Biofilms in the large bowel suggest an apparent function of the human vermiform appendix. Journal of Theoretical Biology, 249(4), 826-831. doi:10.1016/j.jtbi.2007.08.032
16. Hoentjen, F., Welling, G. W., Harmsen, H. J., Zhang, X., Snart, J., Tannock, G. W., . . . Dieleman, L. A. (2005). Reduction of Colitis by Prebiotics in HLA-B27 Transgenic Rats Is Associated with Microflora Changes and Immunomodulation.Inflammatory Bowel Diseases, 11(11), 977-985. doi:10.1097/01.mib.0000183421.02316.d5
17. Filippo, C. D., Cavalieri, D., Paola, M. D., Ramazzotti, M., Poullet, J. B., Massart, S., . . . Lionetti, P. (2010). Impact of diet in shaping gut microbiota revealed by a comparative study in children from Europe and rural Africa. Proceedings of the National Academy of Sciences, 107(33), 14691-14696. doi:10.1073/pnas.1005963107
Foods high in prebiotics image - http://www.nutrientsreview.com/carbs/fiber-prebiotics.html
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