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Review
. 2017 Mar 28;23(12):2124-2140.
doi: 10.3748/wjg.v23.i12.2124.

Diet and microbiota in inflammatory bowel disease: The gut in disharmony

Affiliations
Review

Diet and microbiota in inflammatory bowel disease: The gut in disharmony

Davy C M Rapozo et al. World J Gastroenterol. .

Abstract

Bacterial colonization of the gut shapes both the local and the systemic immune response and is implicated in the modulation of immunity in both healthy and disease states. Recently, quantitative and qualitative changes in the composition of the gut microbiota have been detected in Crohn's disease and ulcerative colitis, reinforcing the hypothesis of dysbiosis as a relevant mechanism underlying inflammatory bowel disease (IBD) pathogenesis. Humans and microbes have co-existed and co-evolved for a long time in a mutually beneficial symbiotic association essential for maintaining homeostasis. However, the microbiome is dynamic, changing with age and in response to environmental modifications. Among such environmental factors, food and alimentary habits, progressively altered in modern societies, appear to be critical modulators of the microbiota, contributing to or co-participating in dysbiosis. In addition, food constituents such as micronutrients are important regulators of mucosal immunity, with direct or indirect effects on the gut microbiota. Moreover, food constituents have recently been shown to modulate epigenetic mechanisms, which can result in increased risk for the development and progression of IBD. Therefore, it is likely that a better understanding of the role of different food components in intestinal homeostasis and the resident microbiota will be essential for unravelling the complex molecular basis of the epigenetic, genetic and environment interactions underlying IBD pathogenesis as well as for offering dietary interventions with minimal side effects.

Keywords: Crohn’s disease; Diet; Epigenetics; Microbiota; Ulcerative colitis.

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Conflict of interest statement

Conflict-of-interest statement: The authors declare that there is no conflict of interest regarding the publication of this paper.

Figures

Figure 1
Figure 1
Schematic model of host-microbiota interactions in the intestine. The interaction between the resident (autochthonous) microbiota and the mucosal immune system is highly complex and, in normal conditions, results in a tolerogenic response. In genetically predisposed individuals, a dysbiotic microbiota, fuelled by environmental factors, particularly dietary constituents, induces pathogenic immune recognition and responses, further compromising the epithelial barrier and defence mechanisms, leading to chronic inflammation, as observed in inflammatory bowel disease.
Figure 2
Figure 2
Interactive biological networks are affected by environmental factors. Environmental exposures, including dietary constituents and a dysbiotic microbiota, affect the host’s genome and epigenome in a redundant and overlapping fashion, determining aberrant immunity and defective intestinal homeostasis, which lead to the development of inflammatory bowel disease.

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