Mediators of Inflammatory Bowel Disease

Digestive Diseases and Sciences

, Volume 33, Issue 3, pp 71S-77S

Neuropeptides, inflammation, and motility

  • Emeran A. MayerAffiliated withDepartment of Medicine, Division of Gastroenterology, Harbor-UCLA Medical CenterCenter for Ulcer Research and EducationHarbor/UCLA Inflammatory Bowel Disease Center
  • , Helen RaybouldAffiliated withDepartment of Medicine, Division of Gastroenterology, Harbor-UCLA Medical CenterCenter for Ulcer Research and EducationHarbor/UCLA Inflammatory Bowel Disease Center
  • , Christian KoelbelAffiliated withDepartment of Medicine, Division of Gastroenterology, Harbor-UCLA Medical CenterCenter for Ulcer Research and EducationHarbor/UCLA Inflammatory Bowel Disease Center

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Abstract

Neurogenic inflammation is a reaction which includes vasodilation, plasma extravasation, and smooth muscle contraction elicited by activation of and release of mediators from unmyelinated afferent nerve endings. Further release of inflammatory mediators follows activation of axon collaterals associated with these afferent nerve endings as axon reflexes. Substance P, somatostatin, vasoactive intestinal polypeptide, and calcitonin generelated peptide are candidate mediators. Recent evidence suggests that several of these peptides may be colocalized either with one or more other peptides or with acetylcholine or noradrenalin. Communicating pathways exist between nerves within the mucosa and the muscle layers. Both long and short visceral reflexes occur. Inflammatory, mechanical, or chemical stimuli reaching the mucosa may release peptides from peripheral nerve endings. Thus neurogenic inflammation may be an important factor in inflammatory bowel disease.

Key words

substance P primary afferent nerves capsaicin