The educational content in this post, elaborated in collaboration with Bromatech, was independently developed and approved by the GMFH publishing team and editorial board.


Have you recently been diagnosed with inflammatory bowel disease? Learn more about the types and symptoms of this debilitating condition

Inflammatory bowel disease (IBD) is a general term used to describe disorders that cause chronic inflammation of the gastrointestinal tract. The two most common forms of IBD are Crohn’s disease and ulcerative colitis.

Crohn’s disease Ulcerative colitis
Can affect any part of the gastrointestinal tract from the mouth to the anus, but most commonly affects the last part of the small intestine and parts of the colon. Only affects the large intestine (colon).
Can affect the three layers of the bowel wall (inner, middle and outer). Affects only the inner lining of the colon.
Some areas of the intestine remain unaffected between patches of diseased intestine. Inflammation affects the intestine evenly.

Atypical forms of IBD include microscopic colitis—an inflammation of the inner lining of the large bowel that can only be seen when a sample of colon tissue is analyzed under a microscope—and pouchitis—an inflammation of the artificial bag or ‘pouch’ created by a surgeon to connect the last part of the small bowel to the anus when the large bowel is removed due to ulcerative colitis or cancer.

Most of the 7 million people with IBD globally suffer in silence. And even though the bowel is the disease’s most affected organ, it can also involve the skin, eyes, liver and muscles. The symptoms of IBD include abdominal pain or swelling in the tummy, recurring or bloody diarrhea, unexplained weight loss, loss of appetite, anemia, fever and tiredness. In children, the disease can result in growth impairment. Emerging evidence also shows that those with Crohn’s disease or ulcerative colitis had higher rates of Alzheimer’s disease and other forms of dementia.

 

Although inflammatory bowel diseases have no specific cause, gut microbiota changes may play an important role in their onset

Crohn’s disease and ulcerative colitis occur through a complex interaction between the environment and our genes. The diseases tend to run in families: between 5% and 20% of patients have a parent, child or sibling who is affected. The disorders can also occur at any age and are becoming more common throughout the world.

Although ulcerative colitis and Crohn’s disease have no specific cause, scientists speculate that the current rise is linked to industrialization and a Western-style diet, rich in meat and processed foods. The idea that living in an overly hygienic environment may lead the immune system to attack its own healthy tissue and fuel intestinal inflammation is also possible. In addition, exposure to different elements such as infectious agents and medications such as nonsteroidal anti-inflammatory drugs can trigger disease onset or make it worse in people who already have it.

Beyond the environment and genetics, the gut microbiota may also be involved. Some studies (here; here; here; here) have observed that people affected with IBD have an altered gut microbiota composition compared to healthy people. For example, the gut microbiota of people with IBD has low microbial diversity, a reduced abundance of protective bacteria such as Bifidobacterium species, Lactobacillus species and Faecalibacterium prausnitzii and a higher abundance of pathogens such as enteropathogenic Escherichia coli.

Beyond bacteria, the fungal microbiota is also altered in IBD. Patients with IBD have higher levels of Candida albicans, and lower levels of Saccharomyces cerevisiae. Also, a yeast found in cheese and cured meat rinds was found in high levels in Crohn’s disease ulcers and perpetuated intestinal inflammation in mice.

Accordingly, the altered bacterial and fungi microbiota in patients with IBD suggests the existence of disease-specific microbial hallmarks as a new potential therapeutic target in the foreseeable future.

Alterations in gut microbiota functions have also been reported in IBD, including increased levels of bile acids involved in dietary fat digestion and absorption and decreases in protective short-chain fatty acids. Specifically, altered levels of human and microbial-origin metabolites have been associated with gut inflammation markers such as fecal calprotectin, which suggests they might be used as an early target before major symptoms manifest.

 

Take-home messages

  • Crohn’s disease and ulcerative colitis are common debilitating conditions that can occur at any age and are becoming more prevalent worldwide.
  • The current rise in inflammatory bowel diseases is linked to industrialization and a Western-style diet, rich in meat and processed foods
  • It is not clear whether the gut microbiota is the cause or effect in IBD. Yet, emerging evidence shows an altered bacterial and fungi microbiota in this common condition that could potentially be used as a future therapeutic target.

 

References:

Crohn’s & Colitis Foundation. Overview of Crohn’s disease. Available on: https://www.crohnscolitisfoundation.org/what-is-crohns-disease/overview

Cruz-Correa M, Giardiello FM, Bayless TM. Atypical forms of inflammatory bowel disease: microscopic colitis and pouchitis. Curr Opin Gastroenterol. 2000; 16(4):343-348. doi: 10.1097/00001574-200007000-00009.

GBD 2017 Inflammatory Bowel Disease Collaborators. The global, regional, and national burden of inflammatory bowel disease in 195 countries and territories, 1990-2017: a systematic analysis for the Global Burden of Disease Study 2017. Lancet Gastroenterol Hepatol. 2020; 5(1):17-30. doi: 10.1016/S2468-1253(19)30333-4.

Zhang B, Wang HE, Bai YM, et al. Inflammatory bowel disease is associated with higher dementia risk: a nationwide longitudinal study. Gut. 2021; 70(1):85-91. doi: 10.1136/gutjnl-2020-320789.

Crohn’s & Colitis Foundation. Causes of Crohn’s disease. Available on: https://www.crohnscolitisfoundation.org/what-is-crohns-disease/causes

Ananthakrishnan AN, Bernstein CN, Iliopoulos D, et al. Environmental triggers in IBD: a review of progress and evidence. Nat Rev Gastroenterol Hepatol. 2018; 15(1):39-49. doi: 10.1038/nrgastro.2017.136.

Andoh A, Kuzuoka H, Tsujikawa T, et al. Multicenter analysis of fecal microbiota profiles in Japanese patients with Crohn’s disease. J Gastroenterol. 2012; 47(12):1298-12307. doi: 10.1007/s00535-012-0605-0.

Joossens M, Huys G, Cnockaert M, et al. Dysbiosis of the faecal microbiota in patients with Crohn’s disease and their unaffected relatives. Gut. 2011; 60(5):631-637. doi: 10.1136/gut.2010.223263.

Darfeuille-Michaud A, Boudeau J, Bulois P, et al. High prevalence of adherent-invasive Escherichia coli associated with ileal mucosa in Crohn’s disease. Gastroenterology. 2004; 127(2):412-421. doi: 10.1053/j.gastro.2004.04.061.

Liu S, Zhao W, Lan P, et al. The microbiome in inflammatory bowel diseases: from pathogenesis to therapy. Protein Cell. 2021; 12(5):331-345. doi: 10.1007/s13238-020-00745-3.

Sokol H, Leducq V, Aschard H, et al. Fungal microbiota dysbiosis in IBD. Gut. 2017; 66(6):1039-1048. doi: 10.1136/gutjnl-2015-310746.

Lavelle A, Sokol H. Gut microbiota-derived metabolites as key actors in inflammatory bowel disease. Nat Rev Gastroenterol Hepatol. 2020; 17(4):223-237. doi: 10.1038/s41575-019-0258-z.