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Neuroscience letters · Jul 1999
Neutralizing antibodies to interleukin 1-receptor reduce pain associated behavior in mice with experimental neuropathy.
- C Sommer, S Petrausch, T Lindenlaub, and K V Toyka.
- Neurologische Klinik der Universität Würzburg, Germany. sommer@mail.uni-wuerzburg.de
- Neurosci. Lett. 1999 Jul 23;270(1):25-8.
AbstractWe investigated whether interleukin-1 (IL-1), a mediator of inflammatory pain, also plays a role in pain induced by nerve injury. Female C57BL/6-mice with a chronic constrictive injury of one sciatic nerve, an established model of neurogenic hyperalgesia and allodynia, were treated with different doses (10-80 microg) of a neutralizing monoclonal rat antibody to IL-1 receptor I (anti-IL-1RI). This antibody dose-dependently reduced thermal hyperalgesia and mechanical allodynia in the animals. Furthermore, immunoreactivity for the proinflammatory cytokine tumor necrosis factor-alpha (TNF) was reduced in mice treated with the highest dose of anti-IL-1RI. Degeneration of myelinated fibers was not altered by any of the treatment schedules. We conclude that IL-1 may be a mediator of hyperalgesia after nerve lesion.
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