The gut-brain axis (GBA) is a bidirectional communication network linking the central nervous system (CNS) and the enteric nervous system (ENS), influencing emotional and cognitive centers with peripheral intestinal functions. Recent research highlights the significant role of gut microbiota in these interactions, which appear to be bidirectional through neural, endocrine, immune, and humoral links. This review summarizes evidence supporting the existence of these interactions and the possible pathophysiological mechanisms involved. Studies using germ-free animal models, probiotics, antibiotics, and infection studies have provided insights into the role of microbiota in GBA. Clinical evidence suggests that dysbiosis is associated with central nervous disorders (e.g., autism, anxiety-depressive behaviors) and functional gastrointestinal disorders (FGIDs), particularly irritable bowel syndrome (IBS). The disruption of GBA in IBS can lead to changes in intestinal motility, secretion, and visceral hypersensitivity. Probiotics and non-systemic antibiotics have been shown to modulate GBA and improve symptoms in IBS patients. The gut-brain axis is influenced by the vagus nerve, which transmits information from the gut to the CNS. Microbiota can also affect GBA through the modulation of intestinal barrier function, sensory nerves, and enteroendocrine cells. Stress-induced changes in gut microbiota composition and function can further disrupt GBA, leading to conditions like FGIDs. Understanding these complex interactions may provide new targeted therapies for neurological and gastrointestinal disorders.The gut-brain axis (GBA) is a bidirectional communication network linking the central nervous system (CNS) and the enteric nervous system (ENS), influencing emotional and cognitive centers with peripheral intestinal functions. Recent research highlights the significant role of gut microbiota in these interactions, which appear to be bidirectional through neural, endocrine, immune, and humoral links. This review summarizes evidence supporting the existence of these interactions and the possible pathophysiological mechanisms involved. Studies using germ-free animal models, probiotics, antibiotics, and infection studies have provided insights into the role of microbiota in GBA. Clinical evidence suggests that dysbiosis is associated with central nervous disorders (e.g., autism, anxiety-depressive behaviors) and functional gastrointestinal disorders (FGIDs), particularly irritable bowel syndrome (IBS). The disruption of GBA in IBS can lead to changes in intestinal motility, secretion, and visceral hypersensitivity. Probiotics and non-systemic antibiotics have been shown to modulate GBA and improve symptoms in IBS patients. The gut-brain axis is influenced by the vagus nerve, which transmits information from the gut to the CNS. Microbiota can also affect GBA through the modulation of intestinal barrier function, sensory nerves, and enteroendocrine cells. Stress-induced changes in gut microbiota composition and function can further disrupt GBA, leading to conditions like FGIDs. Understanding these complex interactions may provide new targeted therapies for neurological and gastrointestinal disorders.