Reciprocal Interaction of Diet and Microbiome in Inflammatory Bowel Diseases

Monika Schaubeck; Dirk Haller


Curr Opin Gastroenterol. 2015;31(6):464-470. 

In This Article

Abstract and Introduction


Purpose of review Diet is an emerging but poorly defined disease modulator in inflammatory bowel diseases (IBDs). Dietary factors exert direct effects on epithelial and immune cells and indirectly modulate immune homeostasis by shaping the intestinal microbiota.

Recent findings The increase in IBD prevalence in industrialized countries is associated with lifestyle changes including diets rich in energy, saturated fats, meat and sugar. Despite the fact that the intestinal ecosystem shows high stability and resilience to short-term perturbations, long-term dietary habits have profound effects on composition and function eventually leading to dysbiosis, that is changes in microbial composition associated with deleterious effects to the host. High-throughput sequencing data generated deeper insights of the intestinal ecosystems related to health and disease. However, the available cohort-studies establish associative relationships between microbiota changes and disease, rather than causality. New mouse models of intestinal inflammation and the possibility to transfer disease-associated microbial consortia state an essential tool to unravel the potential of diet-induced microbial shifts.

Summary This review will discuss new insights of how nutrition or single dietary factors shape the intestinal ecosystem. Furthermore, we want to provide perspectives for clinical translation of this knowledge to treat or prevent IBD.


The cause of inflammatory bowel diseases (IBDs) including Crohn's disease and ulcerative colitis is complex and involves genetic and environmental factors. At present, 200 genetic polymorphisms have been identified to be associated with increased IBD-susceptibility, and there are more to come.[1–3] Many of these were connected to microbial recognition and immune defense, thereby putting microbes into the center of the disease pathogenesis, especially ileal Crohn's disease. Disease concordance in identical-twin studies explains up to 40% of Crohn's disease risk, leading to the general agreement that environmental factors (regarded as the 'exposome') dominate IBD risk and development. Epidemiologic studies showed higher IBD prevalence in industrialized countries and adoption of higher incidence rates in the second generation of immigrants, hinting to the fact that adoption of lifestyle – most likely diet – may be a risk factor for later IBD development.[4–6]

Diet is estimated as an essential exposomal factor that targets inflammation-related mechanisms in the host either directly, or indirectly acting via changes in the structure and function of the intestinal microbiota. Meanwhile, numerous experimental and clinical studies addressed the role of diet in IBD pathogenesis and were recently summarized in comprehensive reviews.[7–9] However, even large prospective cohorts could not identify single nutrients or dietary habits with strong risk association to IBD. The only reliable observation was an increased intake of fat and omega-6 fatty acids (such as linoleic acid) to be associated with increased IBD incidence throughout several cohorts.[10,11] Especially increased intake of omega-6 fatty acids is interesting, as those can be further metabolized to arachidonic acid, a precursor for proinflammatory eicosanoids, which gives a plausible mechanism for the loss of homeostasis. In addition, low intake of dietary fiber was associated with increased risk for Crohn's disease, but not ulcerative colitis in the nurses' health study and EpiCom cohort.[12,13] Fibers are not digestible by the host and metabolized to short-chain fatty acids by the colonic microbiota. Especially, butyrate seems to play an important role as energy substrate and transcriptional regulator at the colonic interface, affecting epithelial barrier integrity and bacterial translocation.[14–17] Reduced abundance in butyrate producers such as Faecalibacterium prausnitzii is associated with disease in many IBD studies.[18–20] This shows that microbes and their metabolites (e.g. from fiber or tryptophan-degradation) elicit proinflammatory or anti-inflammatory host responses, for example by the induction of certain immune-cell subtypes, which result in complex diseases, such as IBD.[21–26]

This clearly indicates that diet does not only exert a direct influence on intestinal immune and epithelial cell functions, but also shapes the intestinal microbial community by generating a milieu that favors the growth and metabolic activity of specific bacteria. The microbiota has a crucial role in the development and maintenance of the host's immune homeostasis.[27,28] Therefore, this review summarizes recent findings to the role of diet in shaping the intestinal microbiota and consecutively IBD development, and focuses on the obstacles in the reciprocal interaction of diet and microbiota (Fig. 1).

Figure 1.

Direct and indirect interaction of diet, microbiota and host. Diet influences the host and microbiota alike by provision of nutrients or creating a specific intestinal milieu. The host is because of lifestage and genetic susceptibility more or less prone to dietary or microbial changes