Digestive Diseases and Sciences

, Volume 33, Supplement 3, pp 71S–77S

Neuropeptides, inflammation, and motility

Authors

  • Emeran A. Mayer
    • Department of Medicine, Division of GastroenterologyHarbor-UCLA Medical Center
    • Center for Ulcer Research and Education
    • Harbor/UCLA Inflammatory Bowel Disease Center
  • Helen Raybould
    • Department of Medicine, Division of GastroenterologyHarbor-UCLA Medical Center
    • Center for Ulcer Research and Education
    • Harbor/UCLA Inflammatory Bowel Disease Center
  • Christian Koelbel
    • Department of Medicine, Division of GastroenterologyHarbor-UCLA Medical Center
    • Center for Ulcer Research and Education
    • Harbor/UCLA Inflammatory Bowel Disease Center
Mediators of Inflammatory Bowel Disease

DOI: 10.1007/BF01538134

Cite this article as:
Mayer, E.A., Raybould, H. & Koelbel, C. Digest Dis Sci (1988) 33: 71S. doi:10.1007/BF01538134

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 Pprimary afferent nervescapsaicin

Copyright information

© Plenum Publishing Corporation 1988