The Microbiota-Gut-Brain Axis in Disorders of Gut-Brain Interaction: Mechanisms and Emerging Therapeutic Strategies.
TL;DR
The authors analyze GBA dysfunction across major DGBIs subtypes (irritable bowel syndrome, functional dyspepsia, and functional abdominal pain syndrome), highlighting microbiota dysbiosis, barrier dysfunction, and central sensitization.
Abstract
Disorders of gut-brain interaction (DGBIs), traditionally termed functional gastrointestinal disorders, affect approximately 15% of adults worldwide and are characterized by chronic digestive symptoms without identifiable structural abnormalities. According to the recently updated Rome V framework, DGBIs are characterized by pathogenic dysregulation of bidirectional communication among the central nervous system, enteric nervous system, and intestinal microbiota. This review examines the anatomical and molecular foundations of gut-brain axis (GBA) communication, emphasizing the roles of microbial metabolites (e.g., short-chain fatty acids and tryptophan derivatives) in neuroimmune modulation and visceral sensitivity. The authors analyze GBA dysfunction across major DGBIs subtypes (irritable bowel syndrome, functional dyspepsia, and functional abdominal pain syndrome), highlighting microbiota dysbiosis, barrier dysfunction, and central sensitization. Current therapies include psychological interventions, neuromodulation, microbiota-targeted approaches, dietary management, and pharmacotherapy; however, treatment responses remain highly heterogeneous across patient populations, highlighting the potential value of biomarker-guided and mechanism based therapeutic approaches. Future paradigms will require multiomics profiling, artificial intelligence, and precision medicine to develop mechanism-based diagnostics and individualized treatments, advancing care from symptom-focused to mechanism-targeted approaches.