Diet in the Pathogenesis and Management of Ulcerative Colitis; A Review of Randomized Controlled Dietary Interventions

Abstract

Epidemiological and experimental studies have suggested that diet is one of the environmental factors that contributes to the onset and pathophysiology of ulcerative colitis. Although many patients suffering from ulcerative colitis attribute their symptoms or disease relapse to dietary factors, only a few well-designed randomized controlled trials have been done to investigate the role of diet in the management of ulcerative colitis. Here, we review the potential mechanisms of the relationship between diet and pathogenesis of ulcerative colitis and summarize randomized controlled dietary interventions that have been conducted in ulcerative colitis patients.

Keywords: diet; inflammatory bowel disease; ulcerative colitis.

Figure 1

Although the exact mechanisms responsible for the association between diet and development of inflammatory bowel disease is unknown, several mechanisms have been suggested. An unhealthy dietary pattern such as a Western diet has been linked to changes in the gut microbiome and epithelial barrier function and seems to have a direct influence on immune function, triggering a pro-inflammatory environment characterized by an imbalance in the T helper 17 (T_H17) cell to regulatory T (T_reg) cell ratio [Adapted with permission [11]].

Figure 2

The relationship between gut microbiota and colonic inflammation in inflammatory bowel disease. Inflammation in colon stimulates production of Interferon gamma (IFN-γ) that eventually generates reactive oxygen species (ROS). ROS make products for anaerobic respiration. These products can be used by facultative anaerobes to outgrow, which leads to decreased bacterial diversity. The dysbiotic microbiota may further stimulate the growth of fungi that can worsen inflammation via chitin and β -glucan antigen-presenting cell (APC) activation of the type 1 T helper (T_H1) pathway. In addition, the microbial dysbiosis is associated with increased bacteriophage richness and abundance, which can affect the bacterial microbiota via gene transfer. DMSO, dimethyl sulfoxide; TMAO, trimethylamine N-oxide. [Adapted with permission [13]].

Figure 3

The role of fiber-derived short chain fatty acids (SCFAs) in regulation of intestinal homeostasis. SCFAs serve as energy substrates for colonocytes. In addition, SCFAs regulate intestinal barrier function and immune system through G-protein-coupled receptors (GPRs) signaling. SCFAs promote the differentiation of regulatory T (Treg) cells and the production of interleukin (IL)-10 through GPR43. Furthermore, SCFA facilitate inflammasome activation in colonic epithelial cells through GPR43, stimulating 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 mucin (MUC)2. DC, dendritic cells; FOXP3, forkhead box P3; HDAC, histone deacetylases; Mϕ, macrophages; TJ, tight junctions. [Adapted with permission [22]].