Journal
NEUROENDOCRINE IMMUNOLOGY IN RHEUMATIC DISEASES: TRANSLATION FROM BASICS TO CLINICS
Volume 1193, Issue -, Pages 60-69Publisher
BLACKWELL PUBLISHING
DOI: 10.1111/j.1749-6632.2009.05301.x
Keywords
joint pain; arthritis; TNF alpha; interleukin-6; cytokines
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The proinflammatory cytokines tumor necrosis factor-alpha (TNF-alpha) and interleuldn-6 (IL-6) not only promote and maintain inflammation, they also contribute to the generation and maintenance of inflammatory pain by acting at nociceptive nerve cells. A large proportion of dorsal root ganglion (DRG) neurons express TNF receptors and receptor units for stimulation with IL-6. In the rat model of antigen-induced arthritis (AIA), neutralization of TNF-alpha by etanercept and infliximab reduced inflammation-evoked mechanical hyperalgesia at the inflamed knee joint. This treatment also attenuated the infiltration of macrophages into the DRGs usually observed during the acute phase of AIA. Intra-articular application of etanercept reduced the responses of C-fibers to mechanical stimulation of the inflamed joint but did not influence responses to stimulation of the normal joint. Finally, in cultured DRG neurons TNF-alpha increased the proportion of neurons that express the TRPV1 receptor and may thus contribute to the generation of inflammation-evoked thermal hyperalgesia.
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