The development of insights into the role of cytokine modulation of pain has been the prototypical story of translational research from mouse to man. Pain has been understood in the context of inflammation associated with tissue injury: nociception in a milieu of an inflammatory soup bathing small nerve fibers following tissue injury. Translational research with mice during the past decade has now revealed that the pathogenesis of neuropathic pain, the devastating pain condition associated with direct injury or disease to the somatosensory nervous system, is also a consequence of inflammation of a type described as cytokine-mediated neuroinflammation regulated by glia and neurons.
In this chapter we will review the current understanding of cytokines in the pathogenesis of pain, and especially neuropathic pain, based on basic science research with rodent models of peripheral nerve injury. This knowledge has expanded understanding of the role of cytokines in neural dysfunction and provided an additional rationale for therapeutic use of anti-cytokine agents in human painful degenerative diseases. Herein, we review recent data to support the concept that the proinflammatory cytokine-driven processes of degeneration are at the basis of the neuropathic pain condition, and that anti-cytokine therapy represents a promising approach to treating human neuropathic pain states. Additionally, we suggest that the relationship between cytokines and matrix metalloproteinases can be therapeutically exploited.
Copyright © 2010 by Taylor and Francis Group, LLC.