肠易激综合征发病机制研究进展

Abstract: Irritable bowel syndrome (IBS) is a prevalent functional gastrointestinal disorder characterized by abdominal pain, bloating, and altered bowel habits, without detectable structural abnormalities. The pathogenesis of IBS is multifactorial, involving abnormal immune activation, disruption of gut microbiota homeostasis, and dysregulation of the brain-gut axis (BGA). Research shows impaired intestinal barrier integrity and chronic low-grade inflammation are considered pivotal factors in disease progression. Dysregulation of immune cells and cytokines contributes to visceral hypersensitivity and motility dysfunction, while microbial imbalance alters metabolic profiles, including short-chain fatty acids (SCFAs) and neurotransmitters, thereby influencing enteric neural activity and brain-gut communication. Psychological stress, anxiety, and depression further exacerbate intestinal dysfunction through neuroendocrine pathways, forming a complex neuro-immune-microbial interaction network. Current therapeutic strategies are shifting from symptom-based pharmacological management to mechanism-driven multidimensional interventions. These include immune and neural modulation through medications, dietary regulation and probiotic supplementation to restore microbial balance, and psychological therapies to stabilize the brain-gut axis. Such integrated, mechanism-oriented approaches aim not only to alleviate symptoms but also to restore gut homeostasis and improve long-term outcomes. Future research should focus on elucidating the cross-talk among immune, microbial, and neural systems, advancing personalized and precision therapies to enhance the long-term management of IBS.