2008
DOI: 10.1002/art.23608
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Antinociceptive effects of tumor necrosis factor α neutralization in a rat model of antigen‐induced arthritis: Evidence of a neuronal target

Abstract: Objective. The reduction of pain in the course of antiinflammatory therapy can result from an attenuation of the inflammatory process and/or from the neutralization of endogenous mediators of inflammation that act directly on nociceptive neurons. The purpose of this study was to investigate whether analgesic effects of the neutralization of tumor necrosis factor ␣ (TNF␣) are due to an attenuation of inflammation or whether direct neuronal effects significantly contribute to pain relief in the course of therapy… Show more

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Cited by 147 publications
(156 citation statements)
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“…The same study provided electrophysiological recordings performed in anesthetized rats showing reduced responses to noxious outward rotation of inflamed knees after etanercept treatment. 34 As mentioned above and shown in Figure 1B, TNF-α enhances the production and release of several other proinflammatory cytokines and factors like IL-6, IL-8, IL-1β, NGF, and prostaglandins and by that amplifies the inflammatory response. The injection of TNF-α into healthy tissue of rats locally elevated the levels of IL-1β and NGF and produced a transient, dose-dependent mechanical hyperalgesia.…”
Section: Pronociceptive Cytokinesmentioning
confidence: 74%
“…The same study provided electrophysiological recordings performed in anesthetized rats showing reduced responses to noxious outward rotation of inflamed knees after etanercept treatment. 34 As mentioned above and shown in Figure 1B, TNF-α enhances the production and release of several other proinflammatory cytokines and factors like IL-6, IL-8, IL-1β, NGF, and prostaglandins and by that amplifies the inflammatory response. The injection of TNF-α into healthy tissue of rats locally elevated the levels of IL-1β and NGF and produced a transient, dose-dependent mechanical hyperalgesia.…”
Section: Pronociceptive Cytokinesmentioning
confidence: 74%
“…For technical reasons (e.g., to monitor painrelated behavior in unrestrained animals), we measured secondary hyperalgesia in the hind paws after induction of AIA in the knee joint. This is valid because primary hyperalgesia in the inflamed knee is usually accompanied by secondary hyperalgesia in the paws (23,24). At 2 time points before AIA induction (baseline), as well as on days 1, 3, 7, 14, and 21 of AIA, secondary mechanical hyperalgesia was determined on ipsilateral and contralateral hind paws, using a dynamic plantar esthesiometer (Ugo Basile).…”
Section: Methodsmentioning
confidence: 99%
“…Secondary thermal hyperalgesia was assessed in the hind paws with an algesiometer (Ugo Basile) as described elsewhere (23). After accommodation of the animals to the testing device, 3 consecutive radiant-heat stimuli were applied to the hind paws with at least 1-minute intervals between stimuli.…”
Section: Methodsmentioning
confidence: 99%
“…In contrast to the well-documented role of TNF-α as a proinflammatory cytokine, its role as a mediator of pain is incompletely characterized. It is known that both receptors for TNF-α are expressed in dorsal root ganglion neurons and that intra-articular injection of TNF-α blocking agents reduces nociception elicited by joint inflammation (10). TNF-α is also involved in development of mechanical hyperalgesia following injury (11,12).…”
Section: Cytokines | Antiinflammatory Therapymentioning
confidence: 99%