Dysbiosis & Inflammatory Bowel Disease (IBD)

Overview

Inflammatory Bowel Disease (IBD) with mucosal inflammation and gastrointestinal symptoms are associated with dysbiosis. The composition of the gut microbiota has been studied concerning the symptoms of stool frequency, rectal bleeding in ulcerative colitis (UC), and abdominal pain and stool frequency in Crohn's disease (CD). In addition, mucosal inflammation was assessed via fecal calprotectin. The data suggest that microbiota may contribute to Inflammatory Bowel Disease (IBD) patients' symptoms and the effects of mucosal inflammation (1, 2, 3, 4, 5, 6, 7).

Inflammatory Bowel Disease (IBD) is one of the most studied diseases in terms of microbial bioactivity leading to dysbiosis (8).

Microbial diversity

Disease specific taxa signatures highlighting a role for Peptostreptococcaceae and within the Ruminococcaceae the genus Gemmiger in Inflammatory Bowel Disease (IBD) (9).

A hallmark of the gut microbiota in Inflammatory Bowel Disease (IBD) is reduced biodiversity, caused by a shift from obligately anaerobic bacteria, including clostridia, to facultative aerobes, such as enterobacteria (10, 11, 12).

In the Inflammatory Bowel Disease (IBD) group, Firmicutes, Proteobacteria, Verrucomicrobia, and Fusobacteria were significantly increased, while Bacteroidetes and Cyanobacteria were decreased. At the genus level, Escherichia, Faecalibacterium, Streptococcus, Sutterella, and Veillonella increased, while Bacteroides, Flavobacterium, and Oscillospira decreased (13).

In Inflammatory Bowel Disease (IBD)-associated dysbiosis, one of the key characteristics is a reduction in bacterial diversity. This is accompanied by an increase in the relative abundance of gram-negative bacteria, especially coliforms, and a decrease in the abundance of Firmicutes (14, 15).

Evidence for the connection between dysbiosis and inflammatory Bowel Disease (IBD)

The premise of diverse microbiome manipulation approaches (prebiotics, probiotics, fecal microbiota transplantation) presumes that reconfiguration of the microbiome toward a more “eubiotic” or less pro-inflammatory profile would lead to a reduction of intestinal inflammation (16).

Dysbiosis - Chicken or Egg?

Even if it is still not conclusively clarified whether the dysbiosis is the cause of the IBD or its consequence, the dysbiosis promotes intestinal inflammation (13, 17).

Alterations in the composition of intestinal microbes have been linked to chronic inflammation for quite some time. However, establishing a definitive cause-and-effect relationship between dysbiosis and inflammatory bowel disease (IBD) has proven challenging, particularly in human studies (18).

Mechanistic consequences of dysbiosis

Dysbiosis and intestinal barrier impairment are associated with the development of a number of chronic inflammatory disorders and systemic diseases (18, 19, 20).

Dysbiosis alters not only the composition of the intestinal microbiota, but also its metabolome, thereby exerting a wide range of effects on the host (18).

Metabolite content and microbiological profiles differed significantly between Inflammatory Bowel Disease (IBD) and healthy subjects (13).

Crohn's disease (CD) and Ulcerative colitis (UC) must be considered differently

Dysbiosis may be involved in the activity of Inflammatory Bowel Disease (IBD) and that there may be differences between patients with Crohn's disease (CD) and Ulcerative colitis (UC) (21).

Three prospective and seven cross-sectional studies (NOS score 6–8) were included. Five studies included patients with Crohn's disease (CD) (231 patients) and eight included patients with Ulcerative colitis (UC) (392 patients). Compared to patients in remission, patients with active Inflammatory Bowel Disease (IBD) had lower abundance of Clostridium coccoides (MD = −0.49, 95% CI: −0.79 to −0.19), Clostridium leptum (MD = −0.44, 95% CI: −0.74 to −0.14), Faecalibacterium prausnitzii (MD = −0.81, 95% CI: −1.23 to −0.39) and Bifidobacterium (MD = −0.37, 95% CI: −0.56 to −0.17). Subgroup analyses showed a difference in all four bacteria between patients with Ulcerative colitis (UC) classified as active or in remission. Patients with active Crohn's disease (CD) had fewer C. leptum, F. prausnitzii and Bifidobacterium, but not C. coccoides (21).

References

(1) Hellmann et al. 2023 Inflammatory Bowel Diseases 29(2): 286-296
(2) Littman & Pamer 2011 Cell Host Microbe. 10: 311-323
(3) Honda & Littman 2012 Annu. Rev. Immunol. 30: 759–795
(4) Pickard et al. 2017 Immunol Rev. 279(1): 70-89
(5) Frank et al. 2007 Proc Natl Acad Sci U S A. 104: 13780–13785
(6) Takaishi et al. 2008 Int J Med Microbiol. 298: 463-472
(7) Sha et al. 2013 Diagn Microbiol Infect Dis. 75: 245-251
(8) Zhang et al. 2022f Nature 606: 754
(9) Volkova & Ruggles 2021
(10) Turnbaugh et al. 2009
(11) Qin et al. 2010 Nature 464: 59-65
(12) Schirmer et al. 2019 Nat. Rev. Microbiol. 17: 497-511
(13) Santoru et al. 2017 Sci Rep. 7: 9523
(14) Tamboli et al. 2004 Gut 53: 1-4
(15) Honda & Littman 2012 Annu. Rev. Immunol. 30: 759–795
(16) Limketkai et al. 2020 Inflamm Bowel Dis. 26: 510-514
(17) Eom et al. 2018
(18) Ni et al. 2017 Nat Rev Gastroenterol Hepatol. 14(10): 573-584
(19) Balzan et al. 2007 J GastroenterolHepatol. 22(4): 464-71
(20) Leaphart & Tepas 3rd 2007 Surgery 141(5): 563-569
(21) Prosberg et al. 2016 Scand J Gastroenterol. 51: 1407-1415

see also:
Bifidobacterium breve & Ulcerative colitis (UC)
Clostridioides (Clostridium) difficile & Inflammatory Bowel Disease (IBD)
Crohn's disease (CD) & Dysbiosis
Desulfovibrio piger
Diseases / Disorders & Dysbiosis
Exclusive Enteral Nutrition (EEN) & Crohn’s Disease (CD)
Gammaproteobacteria & Inflammatory Bowel Disease (IBD)
Gut microbiota & Inflammatory Bowel Disease (IBD)
Gut microbiota & Ulcerative colitis (UC)