The Role of Dietary Nutrients in Inflammatory Bowel Disease

Abstract

Inflammatory bowel disease (IBD) is a chronic and relapsing inflammatory disease of the gastrointestinal tract. Although the precise etiology of IBD remains incompletely understood, accumulating evidence suggests that various environmental factors, including dietary nutrients, contribute to its pathogenesis. Dietary nutrients are known to have an impact on host physiology and diseases. The interactions between dietary nutrients and intestinal immunity are complex. Dietary nutrients directly regulate the immuno-modulatory function of gut-resident immune cells. Likewise, dietary nutrients shape the composition of the gut microbiota. Therefore, a well-balanced diet is crucial for good health. In contrast, the relationships among dietary nutrients, host immunity and/or the gut microbiota may be perturbed in the context of IBD. Genetic predispositions and gut dysbiosis may affect the utilization of dietary nutrients. Moreover, the metabolism of nutrients in host cells and the gut microbiota may be altered by intestinal inflammation, thereby increasing or decreasing the demand for certain nutrients necessary for the maintenance of immune and microbial homeostasis. Herein, we review the current knowledge of the role dietary nutrients play in the development and the treatment of IBD, focusing on the interplay among dietary nutrients, the gut microbiota and host immune cells. We also discuss alterations in the nutritional metabolism of the gut microbiota and host cells in IBD that can influence the outcome of nutritional intervention. A better understanding of the diet-host-microbiota interactions may lead to new therapeutic approaches for the treatment of IBD.

Keywords: diet; immunity; inflammatory bowel disease (IBD); intestinal barrier; microbiota.

Figure 1

The role of dietary amino acids in intestinal homeostasis. Dietary tryptophan is metabolized to kynurenine or indole derivatives by host cells or the gut microbiota, respectively. Kynurenine promotes the differentiation of Treg and induces IL-10 production by Treg cells through AhR. Lactobacillus species are capable of catabolizing tryptophan into indole derivatives that are ligands for the AhR. Activation of AhR in gut-resident T cells and ILC enhances production of IL-22, which in turn potentiates mucosal barrier integrity. Arginine and glutamine metabolism in intestinal epithelial cells is associated with epithelial barrier and intestinal wound repair. Arginine also plays an important role of the immune system. Arginine is catabolized by iNOS in M1 macrophages and by arginase II in M2 macrophages. The arginine metabolisms regulate anti-microbial and -tumor activity and immune suppression in M1 and M2 macrophages, respectively.

Figure 2

Dietary fiber-derived SCFAs regulate intestinal homeostasis. Dietary fiber-derived SCFAs serve as energy substrates for colonocytes. Likewise, SCFAs regulate intestinal barrier function and immune system through GPCRs signaling. SCFAs promote the differentiation into Treg cells and the production of IL-10 from Treg cells through GPR43. SCFA facilitate inflammasome activation in colonic epithelial cells through GPR43, resulting in an IL-18 production that is critical for anti-inflammation and epithelial repair. SCFAs also regulate intestinal barrier function via enhancing the expression of tight junction proteins and the synthesis of MUC2.