Neutralizing antibodies to interleukin 1-receptor reduce pain associated behavior in mice with experimental neuropathy.
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 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.
Sommer
C
C
Neurologische Klinik der Universität Würzburg, Germany. sommer@mail.uni-wuerzburg.de
Petrausch
S
S
Lindenlaub
T
T
Toyka
K V
KV
D000818:Animals; D000911:Antibodies, Monoclonal / Q000494:pharmacology*; D005260:Female; D006930:Hyperalgesia / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control; D051379:Mice; D008810:Mice, Inbred C57BL; D009410:Nerve Degeneration / Q000473:pathology / Q000503:physiopathology; D009412:Nerve Fibers / Q000473:pathology / Q000502:physiology; D009437:Neuralgia / Q000473:pathology / Q000503:physiopathology* / Q000517:prevention & control; D051381:Rats; D017472:Receptors, Interleukin-1 / Q000276:immunology / Q000502:physiology*; D012584:Sciatic Nerve / Q000293:injuries / Q000473:pathology / Q000503:physiopathology*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D000911:Antibodies, Monoclonal; D017472:Receptors, Interleukin-1; D014409:Tumor Necrosis Factor-alpha