Gut Microbiota in Inflammatory Bowel Diseases (IBD)

Reginold Sivarajan, BSc Microbiology and Immunology
Contributor

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PHOTO:Team, GMFH Editing, and Kristina Campbell. "Gut Microbiota Studies Lead to New Understandings of IBD." Gut Microbiota for Health. N.p., 02 Mar. 2016. Web.

Inflammatory bowel disease (IBD), including Crohn's disease (CD) and ulcerative colitis (UC) affects approximately 1.5 million Americans and the incidence seems to be increasing worldwide (1). The development of the IBD disease is currently thought to involve an inappropriate and persistent inflammatory response to commensal gut microbes (relationship between two organisms where one organism, the bacteria in this case, benefits from the human host without affecting it) in genetically susceptible individuals. Although host genetics play a critical role in disease pathogenesis, concordance rates in monozygotic twins of 16% for ulcerative colitis and about 35% for Crohn's disease indicate that non-genetic factors play a substantial role in the development of IBD (4) 

The notion that the gut microbiota plays a critical role in the development of IBD is supported by a multitude of animal studies showing that bacterial colonization of the gut is critical for the development of intestinal inflammation (2). Clinical observations in patients with IBD also support a role for the gut microbiota (bacteria that harbours the gut) since IBD usually affects intestinal regions with the highest level of bacteria, and both fecal diversion and the use of antibiotics can be effective in the management of Crohn's disease (3). 

Population-based studies suggest that IBD is unevenly distributed throughout the world with the highest disease rates occurring in industrialized nations (5). A “Westernized” diet rich in animal fat and protein while low in fiber, may alter the gut microbiome in a way that increases the risk for the development of IBD. The development of a “dysbiotic” microbiome (population of bacteria in human host) has, indeed, been the source of speculation as an etiologic factor in disease pathogenesis (6). 

What can you do?

• High dietary intake of total fats, polyunsaturated fatty acids (PUFAs), omega-6 fatty acids, and meat are associated with an increased risk of CD and UC (7).
• High fiber and fruit intakes are associated with a decreased CD risk; and high vegetable intake are associated with a decreased UC risk (7).

Additional Resources:

• If you want to learn more about the Gut Microbiota follow us on our instagram page the thegutguys
• If you want to learn more about Inflammatory bowel disease (IBD) follow our good friends ibddolls

(1)Molodecky NA, Soon IS, Rabi DM, Ghali WA, Ferris M, Chernoff G, Benchimol EI, Panaccione R, Ghosh S, Barkema HW, Kaplan GG. Increasing incidence and prevalence of the inflammatory bowel diseases with time, based on systematic review. Gastroenterology. 2012;142:46–54 e42.
(2)Sartor RB. Mechanisms of disease: pathogenesis of Crohn's disease and ulcerative colitis. Nat Clin Pract Gastroenterol Hepatol. 2006;3:390–407.
(3)Harper PH, Lee EC, Kettlewell MG, Bennett MK, Jewell DP. Role of the faecal stream in the maintenance of Crohn's colitis. Gut. 1985;26:279–84. 
(4)Spehlmann ME, Begun AZ, Burghardt J, Lepage P, Raedler A, Schreiber S. Epidemiology of inflammatory bowel disease in a German twin cohort: results of a nationwide study. Inflamm Bowel Dis. 2008;14:968–76
(5)Molodecky NA, Soon IS, Rabi DM, Ghali WA, Ferris M, Chernoff G, Benchimol EI, Panaccione R, Ghosh S, Barkema HW, Kaplan GG
Gastroenterology. 2012 Jan; 142(1):46-54.e42; quiz e30.
(6)Sartor RB. Microbial influences in inflammatory bowel diseases. Gastroenterology. 2008;134:577–94.
(7)Hou JK, Abraham B, El-Serag H. Dietary intake and risk of developing inflammatory bowel disease: a systematic review of the literature. Am J Gastroenterol. 2011;106:563–73.