Inflammatory bowel diseases (IBD), including Crohn's disease (CD) and ulcerative colitis (UC), are chronic inflammatory disorders of the gastrointestinal tract. The pathogenesis of IBD involves genetic predisposition, environmental factors, aberrant immune responses, and a disturbed gut microbiota. Recent studies using gnotobiotic models, genome-wide association studies, and epidemiological data support the role of the gut microbiota in IBD. Both CD and UC are characterized by severe dysbiosis, marked by an expansion of harmful bacteria and depletion of beneficial ones. Specific bacterial genera involved in short-chain fatty acid production, bile acid transformation, and tryptophan metabolism are reduced, while members of the phyla Proteobacteria and Actinobacteria are increased. This imbalance leads to exaggerated immune responses and altered metabolomic profiles, contributing to inflammation. The review highlights bacterial dysbiosis across different intestinal sites and their metabolomic impacts in IBD. IBD is associated with a loss of beneficial gut microbiota and an increase in pathobionts. The gut microbiome plays a crucial role in maintaining intestinal homeostasis, with the gastrointestinal tract being the most densely inhabited site. The human microbiome, comprising bacteria, viruses, fungi, protozoa, and archaea, is a functional extension of the host genome. The gut microbiome is influenced by factors such as diet, smoking, and antibiotics. Dysbiosis in IBD is characterized by reduced diversity and loss of beneficial bacteria, with increased pathobionts. Studies using gnotobiotic models and twin studies suggest that gut microbiota may precede IBD onset. However, some studies suggest that dysbiosis may be a consequence of IBD-associated inflammation. The gut microbiome is a key factor in IBD pathogenesis, with dysbiosis contributing to immune dysregulation and inflammation. The review emphasizes the clinical relevance of these findings in understanding and managing IBD.Inflammatory bowel diseases (IBD), including Crohn's disease (CD) and ulcerative colitis (UC), are chronic inflammatory disorders of the gastrointestinal tract. The pathogenesis of IBD involves genetic predisposition, environmental factors, aberrant immune responses, and a disturbed gut microbiota. Recent studies using gnotobiotic models, genome-wide association studies, and epidemiological data support the role of the gut microbiota in IBD. Both CD and UC are characterized by severe dysbiosis, marked by an expansion of harmful bacteria and depletion of beneficial ones. Specific bacterial genera involved in short-chain fatty acid production, bile acid transformation, and tryptophan metabolism are reduced, while members of the phyla Proteobacteria and Actinobacteria are increased. This imbalance leads to exaggerated immune responses and altered metabolomic profiles, contributing to inflammation. The review highlights bacterial dysbiosis across different intestinal sites and their metabolomic impacts in IBD. IBD is associated with a loss of beneficial gut microbiota and an increase in pathobionts. The gut microbiome plays a crucial role in maintaining intestinal homeostasis, with the gastrointestinal tract being the most densely inhabited site. The human microbiome, comprising bacteria, viruses, fungi, protozoa, and archaea, is a functional extension of the host genome. The gut microbiome is influenced by factors such as diet, smoking, and antibiotics. Dysbiosis in IBD is characterized by reduced diversity and loss of beneficial bacteria, with increased pathobionts. Studies using gnotobiotic models and twin studies suggest that gut microbiota may precede IBD onset. However, some studies suggest that dysbiosis may be a consequence of IBD-associated inflammation. The gut microbiome is a key factor in IBD pathogenesis, with dysbiosis contributing to immune dysregulation and inflammation. The review emphasizes the clinical relevance of these findings in understanding and managing IBD.