Visceral pain perception
Preclinical studies suggest that the perception of visceral pain can be influenced by gut microbiota.20-23 In animal models of visceral pain induced by dysbiosis, interventions targeting the gut microbiome have been shown to improve pain responses.20,23 Moreover, one study reported visceral hypersensitivity development in rats that received fecal microbiota transplants from patients with IBS.22
Recent data have shown that gut dysbiosis may cause local or systemic immune activation, which can contribute to visceral hypersensitivity by disrupting epithelial barrier function.4,24 Altered fermentation due to microbial imbalance and gut bacteria modulation of intestinal sensory nerve endings may also contribute to visceral hypersensitivity.24
Altered Fermentation
Increased bacterial fermentation of poorly absorbable carbohydrates resulting from alterations in gut microbial composition contributes to the production of excessive intestinal gases. These gases can cause bloating, flatulence, abdominal pain, and distension.4-7 Additionally, increased production of methane gas has been associated with constipation in IBS-C and increased production of hydrogen gas has been associated with diarrhea in IBS-D.7
Altered GI Motility
The gut microbiota play a critical role in regulating serotonin (5-HT) levels in the colon and systemic circulation.25 Changes in microbial composition can increase the production of both short-chain fatty acids and 5-HT.1,6,7,25 The resulting colonic contraction, increased motility, accelerated intestinal transit, and changes in water and electrolyte transport contribute to the development of diarrhea.1,6,7 Certain intestinal bacteria can also suppress intestinal motility, resulting in constipation through the metabolites they produce.26
Altered Barrier Function and Immune System Activation
Microbial imbalance can contribute to increased intestinal permeability and immune system activation.1,4,27,28 These changes may lead to inflammatory cell infiltration and the release of cytokines or chemokines that interact with the intestinal environment to cause abdominal pain and diarrhea.1,4,29
Disrupted Signaling Along the Gut-Brain Axis
The microbiome-gut-brain axis enables bidirectional communication between the gut microbiota, enteric nervous system, and central nervous system. These neural pathways connect cognitive and emotional activity with peripheral intestinal functions.1,27,30
Changes in cognition and behavior have been observed as a result of disrupted communication between the gut and brain due to dysbiosis.1,25,27,31 According to animal studies, this disruption is caused by the release of inflammatory mediators and neuroactive substances into the systemic circulation. Psychological stress is thought to further influence mucosal immunity, gut microbiota, and gut barrier function, which may perpetuate symptoms similar to those experienced by patients with IBS.25,31,32