Inflammatory mediators and modulators of pain

Stephen McMahon, David Bennett, Stuart Bevan

    Research output: Chapter in Book/Report/Conference proceedingChapter


    Disease and injury frequently result in pain and hyperalgesia. These abnormal sensory events arise in part from the action of inflammatory mediators on the peripheral terminals of nociceptive neurons. In this chapter we begin to by reviewing the different ways in which such mediators bring about the activation and sensitization of nociceptive terminals. We then consider the biological effects and potential importance of different inflammatory mediators. The list of mediators has been steadily increasing and includes not only traditionally recognised molecules such as arachidonic acid metabolites and bradykinin but also other small molecules such as ATP and NO. Additionally, evidence has accumulated for an important role of a series of inflammatory cytokines and chemokines such as TNF and Il1, and growth factors , particularly NGF and BDNF, which are all capable of changing the response properties of pain-signalling neurons. They achieve this in a variety of ways, including the activation or sensitization of nociceptive terminals but also the regulation of gene expression by nociceptors. Immune cells are an important source of inflammatory mediators, cytokines and some growth factors. Recently it has become clear that they modulate pain processing not just by the release of mediators into peripherally damaged tissue, but also by the release of the same mediators into the CNS.
    Original languageEnglish
    Title of host publicationWall and Melzack's textbook of pain
    PublisherElsevier Churchill Livingstone
    Pages49 - 72
    Number of pages24
    Publication statusPublished - 2006


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