Diet–microbiota interactions in inflammatory bowel disease
Accumulating evidence suggests that the gut microbiota plays pivotal roles in the regulation of intestinal homeostasis and IBD pathogenesis.
Inflammatory bowel disease (IBD), which includes ulcerative colitis (UC) and Crohn’s disease (CD), is a chronic and relapsing inflammatory disorder of the gastrointestinal tract. The prevalence of IBD has been increasing worldwide, affecting about 3 million people in the United States and 2.5 million people in Europe.
Although the precise etiology of IBD has not yet been defined, it is widely accepted that the confluence of multiple factors, including genetic and environmental factors, is associated with its pathogenesis.
Genetic studies have identified over 200 host genetic loci associated with the risk of IBD, and mostly related to immunological pathways, including innate and adaptive immune responses and autophagy.
The prevalence of IBD is high in Western countries; however, the rates of IBD are also rising in many newly industrialised countries as they become more westernised. For example, the number of IBD patients has increased approximately 20-fold in the past 30 years in Japan. This exponential increase suggests that environmental exposures also play critical roles in the development of IBD.
Among environmental factors, diet, smoking, stress, sleep patterns, hygiene, and antibiotic usage are considered to contribute to the risk of IBD. In particular, diet is widely thought to have a pivotal role in the pathogenesis of IBD. It is well-known that diet shapes the composition of the gut microbiota. Gut microbes use diet-derived nutrients for their growth and colonisation in the gut. In contrast, host cells use microbial metabolites as energy sources and immunomodulatory agents to maintain intestinal homeostasis.
This symbiotic relationship between the gut microbiota and the host is crucial for human health. However, the intake of certain diets, such as the westernised diet characterised by high fat and low fibre, results in gut dysbiosis, thereby disrupting intestinal homeostasis and promoting inflammation of the gut. Gut inflammation, in turn, influences the composition and function of the gut microbiota.
In this review, we discuss the complex reciprocal interactions between diet and the gut microbiota in the context of IBD. In particular, we focus on the metabolic reprogramming of host and microbial cells during inflammation and how these metabolic changes may optimise dietary interventions. We also highlight the future direction of microbiota-targeted dietary interventions to develop precision nutrition for the treatment of IBD.
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