Elsevier

Neuroscience Letters

Volume 270, Issue 1, 23 July 1999, Pages 25-28
Neuroscience Letters

Neutralizing antibodies to interleukin 1-receptor reduce pain associated behavior in mice with experimental neuropathy

https://doi.org/10.1016/S0304-3940(99)00450-4Get rights and content

Abstract

We 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 μg) 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-α (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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Acknowledgements

We would like to thank B. Dekant and L. Biko for technical assistance. This work was supported by Deutsche Forschungsgemeinschaft So 328/2–1 and SFB 353. Presented in part at the Meeting of the Society for Neuroscience, Nov 10, 1998.

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