title: Neuroinflammation in inflammatory bowel disease.
abstract: Inflammatory bowel disease is a chronic intestinal inflammatory condition, the pathology of which is incompletely understood. Gut inflammation causes significant changes in neurally controlled gut functions including cramping, abdominal pain, fecal urgency, and explosive diarrhea. These symptoms are caused, at least in part, by prolonged hyperexcitability of enteric neurons that can occur following the resolution of colitis. Mast, enterochromaffin and other immune cells are increased in the colonic mucosa in inflammatory bowel disease and signal the presence of inflammation to the enteric nervous system. Inflammatory mediators include 5-hydroxytryptamine and cytokines, as well as reactive oxygen species and the production of oxidative stress. This review will discuss the effects of inflammation on enteric neural activity and potential therapeutic strategies that target neuroinflammation in the enteric nervous system.
authors.affiliation: Global Neuroscience Initiative Foundation, Los Angeles, CA, USA. slakhan@gnif.org
authors.forename: Shaheen E
authors.initials: SE
authors.lastname: Lakhan
authors.forename: Annette
authors.initials: A
authors.lastname: Kirchgessner
mesh_terms: D000818:Animals; D016923:Cell Death / Q000502:physiology; D017615:Enteric Nervous System / Q000276:immunology / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D007249:Inflammation / Q000276:immunology / Q000473:pathology*; D015212:Inflammatory Bowel Diseases / Q000276:immunology* / Q000473:pathology* / Q000628:therapy; D007422:Intestines / Q000294:innervation / Q000473:pathology / Q000502:physiology / Q000503:physiopathology; D018384:Oxidative Stress; D017981:Receptors, Neurotransmitter / Q000378:metabolism; D015398:Signal Transduction / Q000502:physiology
chemical_list: D017981:Receptors, Neurotransmitter