People with irritable bowel syndrome (IBS) and inflammatory bowel disease (IBD) have different types and amounts of gut bacteria. IBD is linked to fewer overall bacterial species and less of a...
Mechanism
Synthesis from 1 study
In IBD, the gut loses helpful bacteria that protect the lining, allowing harmful ones to invade and cause long-term swelling. In IBS, different bacteria grow too much and make gases and chemicals that irritate nerves and slow or speed up digestion, causing pain and bowel changes—without the same...
Most probable mechanism
In both IBD and IBS, the balance of gut bacteria is disrupted, but in different ways. In IBD, good bacteria that feed the gut lining die off, weakening the barrier and reducing protective signals, which lets harmful bacteria invade and trigger long-lasting inflammation. In IBS, bad bacteria that make gases and toxins multiply, which slow down or speed up the gut and directly irritate nerves, causing pain and changes in bowel movements. Both conditions involve a leaky gut, but in IBD it leads to tissue damage, while in IBS it leads to nerve sensitivity without visible damage.
Reduced abundance of fiber-fermenting bacteria, such as Faecalibacterium prausnitzii, decreases production of short-chain fatty acids like butyrate.
Lower short-chain fatty acid levels impair activation of epithelial receptors and reduce NLRP3 inflammasome activity, leading to decreased interleukin-18 production and weakened mucosal immune defense.
Reduced short-chain fatty acids and expansion of mucus-degrading bacteria downregulate expression of tight junction proteins, increasing intestinal permeability.
Microbial components such as lipopolysaccharide and flagellin translocate across the compromised barrier, activating Toll-like receptors on immune cells and triggering low-grade NF-kB-mediated inflammation.
In IBD, adherent-invasive Escherichia coli binds to overexpressed receptors on epithelial cells, invades the tissue, evades autophagy due to genetic defects, and forms intracellular communities that sustain chronic inflammation.
In IBS, overgrowth of methanogenic archaea produces methane, which directly inhibits intestinal smooth muscle contraction, slowing transit and causing constipation.
In IBS, hydrogen sulfide-producing bacteria increase hydrogen sulfide levels, which activates TRPA1 receptors on sensory nerves, inducing pain and increasing paracellular permeability.
Microbial antigens translocate and activate mast cells near sensory nerves, releasing histamine and nerve growth factor that sensitize afferent nerves and induce neuroplasticity.
In IBS, microbial metabolism shifts toward tryptamine production from tryptophan, which activates serotonin receptors on enteric neurons, increasing motility and secretion.
In IBD, tryptophan is diverted into the kynurenine pathway, reducing serotonin synthesis and altering gut motility and immune regulation.
Less supported by current evidence, but not ruled out
After a severe gut infection, the immune system makes antibodies that mistakenly attack a protein in the gut's nerve network, damaging the cells that control gut movement, leading to slow transit and bacterial overgrowth.
Infectious bacteria produce a toxin that resembles a human nerve protein called vinculin.
The immune system generates antibodies against the bacterial toxin that also bind to vinculin in the enteric nervous system.
These antibodies damage interstitial cells of Cajal and enteric neurons, disrupting the coordinated wave of contractions that move contents through the gut.
Loss of this coordination causes intestinal stasis, bacterial overgrowth, and symptoms of IBS.
When gut bacteria that process bile acids are reduced, primary bile acids build up and secondary bile acids drop, which reduces signals that calm inflammation and increase nerve sensitivity in the gut.
Dysbiosis reduces bacteria that convert primary bile acids into secondary bile acids.
Lower levels of secondary bile acids reduce activation of receptors that normally suppress inflammation and regulate nerve signaling.
Diminished receptor signaling weakens anti-inflammatory pathways and increases sensitivity of gut nerves to stimuli.
Evidence from Studies
Supporting (1)
Community contributions welcome
Gut Microbiota in Irritable Bowel Syndrome and Inflammatory Bowel Disease: Differences in Pathophysiology, Biomarkers, and Treatment Implications
Contradicting (0)
Community contributions welcome
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