Dysbiosis & Inflammatory Bowel Disease (IBD)

How Dysbiosis Relates to Inflammatory Bowel Disease (IBD) Symptoms and Inflammation

Inflammatory Bowel Disease (IBD), characterized by mucosal inflammation and Gastrointestinal symptoms, is associated with dysbiosis. The composition of the gut microbiota has been studied in relation to stool frequency, rectal bleeding in ulcerative colitis (UC), and abdominal pain and stool frequency in Crohn's disease (CD). Mucosal inflammation has also been assessed using fecal calprotectin. The data suggest that microbiota may contribute to IBD symptoms and the effects of mucosal inflammation (1, 2, 3, 4, 5, 6, 7). IBD is among the most extensively studied diseases in relation to microbial bioactivity and dysbiosis (8).

Inflammatory Bowel Disease (IBD): Microbial Signatures and Reduced Diversity

Disease-specific taxa signatures highlight a possible role for Peptostreptococcaceae and the Ruminococcaceae genus Gemmiger in IBD (9).
A hallmark of gut microbiota in 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 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).

Bacterial Shifts Characterize Inflammatory Bowel Disease (IBD)-Associated Dysbiosis

A key characteristic of IBD-associated dysbiosis is a reduction in bacterial diversity. This is accompanied by increased relative abundance of gram-negative bacteria, especially coliforms, and decreased abundance of Firmicutes (14, 15).

Microbiome Therapies Aim to Reduce Gut Inflammation

The premise of diverse microbiome manipulation approaches - including prebiotics, probiotics, and fecal microbiota transplantation - is that reconfiguring the microbiome toward a more “eubiotic”, or less pro-inflammatory, profile may reduce intestinal inflammation (16).
It remains unclear whether dysbiosis is a cause or consequence of IBD. However, dysbiosis may promote intestinal inflammation (13, 17).

Dysbiosis Affects the Gut Barrier and Microbial Metabolome

Alterations in the composition of intestinal microbes have long been linked to chronic inflammation. Establishing a definitive cause-and-effect relationship between dysbiosis and IBD remains challenging, particularly in human studies (18).
Dysbiosis and intestinal barrier impairment are associated with chronic inflammatory disorders and systemic diseases (18, 19, 20). Dysbiosis alters not only the composition of the intestinal microbiota but also its metabolome, exerting a wide range of effects on the host (18). Metabolite content and microbiological profiles differed significantly between people with IBD and healthy subjects (13).

Microbial Patterns Differ Between Crohn’s Disease and Ulcerative colitis (UC)

Dysbiosis may be involved in IBD activity, with 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 (231 patients), and eight included patients with Ulcerative colitis (392 patients).

Active Inflammatory Bowel Disease (IBD) Shows Lower Levels of Beneficial Bacteria

Compared with patients in remission, patients with active 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 found differences in all four bacteria between patients with active or remitting Ulcerative colitis. Patients with active Crohn's disease had fewer C. leptum, F. prausnitzii, and Bifidobacterium, but not C. coccoides (21).

Host-Microbiota Networks May Explain Inflammatory Bowel Disease (IBD) Better

IBD cannot be explained solely by the presence of specific bacteria. The host-microbiota interactome is crucial: it includes microbial composition, genes, gene activity, proteins, metabolites, the intestinal barrier, and immune responses. Only combined analysis of metagenomics, transcriptomics, proteomics, metabolomics, host genetics, and clinical data can uncover more reliable disease mechanisms and support better biomarkers and more individualized IBD therapies. IBD research must move beyond describing dysbiosis to identifying causal, multilayered host–microbe networks and validating them in well-standardized, longitudinal cohorts (22).

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 Gastroenterol Hepatol. 22(4): 464–471
(20) Leaphart & Tepas 3rd 2007 Surgery 141(5): 563-569
(21) Prosberg et al. 2016 Scand J Gastroenterol. 51: 1407-1415
(22) Su et al. 2025 Gut Microbes 17(1)

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)