The article reviews the current understanding of the relationship between inflammatory bowel disease (IBD) and gut microbiota dysbiosis. While there is a general consensus that IBD is associated with changes in the intestinal microbiota, the direct causal relationship between dysbiosis and IBD remains to be established in humans. The review discusses the role of the gut microbiota in specific animal models of colitis and explores potential microbiota-focused interventions for human IBD. Key findings include: 1. **Microbiota Composition and IBD**: Studies show differences in gut microbiota composition between IBD patients and healthy individuals, with reduced diversity and shifts in the balance between commensal and potentially pathogenic microorganisms. However, the precise role of dysbiosis in IBD pathogenesis is unclear, as it could be a consequence of inflammation rather than a cause. 2. **Non-bacterial Microbiota and IBD**: The role of fungi and viruses in IBD is also discussed. Changes in the gut virome and mycobiome have been observed in IBD patients, but their direct causal role remains to be established. 3. **Microbial Metabolites and IBD**: Alterations in microbial metabolites, such as short-chain fatty acids and bile acids, are associated with IBD. These metabolites play a role in immune regulation and inflammation. 4. **Host Mucosal Immune System and Animal Models**: Animal models of colitis have revealed complex immune-microbiota interactions, highlighting the importance of the gut microbiota in maintaining mucosal homeostasis and immune tolerance. 5. **Clinical Studies**: Clinical studies in humans support the role of dysbiosis in IBD pathogenesis, but the lack of prospective data limits definitive conclusions. Interventions such as probiotics, antibiotics, enteral nutrition, and fecal microbiota transplantation (FMT) have shown mixed results. 6. **Conclusion**: The relationship between dysbiosis and IBD is likely complex and dynamic. Further research is needed to define host-microbial interactions and develop effective therapeutic strategies.The article reviews the current understanding of the relationship between inflammatory bowel disease (IBD) and gut microbiota dysbiosis. While there is a general consensus that IBD is associated with changes in the intestinal microbiota, the direct causal relationship between dysbiosis and IBD remains to be established in humans. The review discusses the role of the gut microbiota in specific animal models of colitis and explores potential microbiota-focused interventions for human IBD. Key findings include: 1. **Microbiota Composition and IBD**: Studies show differences in gut microbiota composition between IBD patients and healthy individuals, with reduced diversity and shifts in the balance between commensal and potentially pathogenic microorganisms. However, the precise role of dysbiosis in IBD pathogenesis is unclear, as it could be a consequence of inflammation rather than a cause. 2. **Non-bacterial Microbiota and IBD**: The role of fungi and viruses in IBD is also discussed. Changes in the gut virome and mycobiome have been observed in IBD patients, but their direct causal role remains to be established. 3. **Microbial Metabolites and IBD**: Alterations in microbial metabolites, such as short-chain fatty acids and bile acids, are associated with IBD. These metabolites play a role in immune regulation and inflammation. 4. **Host Mucosal Immune System and Animal Models**: Animal models of colitis have revealed complex immune-microbiota interactions, highlighting the importance of the gut microbiota in maintaining mucosal homeostasis and immune tolerance. 5. **Clinical Studies**: Clinical studies in humans support the role of dysbiosis in IBD pathogenesis, but the lack of prospective data limits definitive conclusions. Interventions such as probiotics, antibiotics, enteral nutrition, and fecal microbiota transplantation (FMT) have shown mixed results. 6. **Conclusion**: The relationship between dysbiosis and IBD is likely complex and dynamic. Further research is needed to define host-microbial interactions and develop effective therapeutic strategies.