<unk><unk><unk>  is caused by a complex interaction of various factors such as intrinsic gastrointestinal factors, CNS dysregulation and psychosocial factors, genetic, and environmental factors. Intrinsic gastrointestinal factors include motor abnormalities, visceral hypersensitivity, immune activation, mucosal inflammation, altered gut microbiota, and abnormal serotonin pathways. Visceral hypersensitivity refers to a decreased threshold for the perception of visceral stimuli that affects spinal excitability, brain stem and cortical modulation, activation of specific gastrointestinal mediators, and recruitment of peripheral silent nociceptors. Immune activation and mucosal inflammation involves an interaction of lymphocytes, mast cells, and proinflammatory cytokines. Environmental factors encompass dietary changes and infections. Psychosocial factors such as stress, anxiety, and depression directly shape adult connectivity in the executive control network consisting of structures such as the insula, anterior cingulate cortex, and the thalamus. Semipermanent or permanent changes in complex neural circuits lead to central pain amplification contributing to abdominal pain in IBS patients. The dorsolateral prefrontal cortex activity (responsible for vigilance and alertness of the human brain) and the mid-cingulate cortex (engaged in attention pathways and responses) is reduced in IBS patients. This reduction may lead to alterations in the subjective sensations of pain. Genetic factors also play a role in IBS. IBS has a high twin concordance and familial aggregation. IBS is associated with single nucleotide polymorphisms (SNPs) in genes involved in immune activation, neuropeptide hormone function, oxidative stress, nociception, permeability of the GI tract, host-microbiota interaction, inflammation, and TNF activity.
Irritable bowel syndrome pathophysiology
Ischemic colitis pathophysiology
Allergic colitis pathophysiology
Stomatitis pathophysiology
Ulcerative colitis pathophysiology
Helicobacter pylori infection pathophysiology
Crohn's disease pathophysiology
H.pylori gastritis pathophysiology