title: Neurophysiologic changes in lumbar nerve root inflammation in the rat after treatment with cytokine inhibitors. Evidence for a role of interleukin-1.
abstract: METHODS
  The present study was designed to evaluate the effect of cytokine inhibitors in experimental allergic radiculitis.
  
  
  OBJECTIVE
  Evaluation of the effect of cytokine inhibitors in experimental allergic radiculitis.
  
  
  BACKGROUND
  A number of cytokines are known to be involved in hyperalgesia and may play a role in radiculitis. Corticosteroids and other cytokine inhibitors antagonize their effects.
  
  
  METHODS
  Experimental allergic radiculitis was induced in rats by injection of bovine myelin from the peripheral nervous system. The sham group subsequently received saline injections; the treatment groups received either prednisolone or interleukin-1 receptor antagonist. Treatment effect was assessed on the basis of motor performance and neurophysiologic parameters.
  
  
  RESULTS
  Treatment ameliorated the symptoms of experimental allergic radiculitis. Prednisolone appeared to be somewhat more effective than interleukin-1 receptor antagonist.
  
  
  CONCLUSIONS
  Because interleukin-1 receptor antagonist specifically blocks the effects of interleukin-1 at its receptors, the present results imply that interleukin-1 is a causal factor in the model of experimental radiculitis used. Its specificity and apparent lack of side effects make interleukin-1 receptor antagonist an attractive candidate treatment for the human disease.
authors.affiliation: Forschungsgruppe Neuroorthopädie, Hemrich-Heine-Universität Düsseldorf, Germany.
authors.forename: P
authors.initials: P
authors.lastname: Wehling
authors.forename: S J
authors.initials: SJ
authors.lastname: Cleveland
authors.forename: K
authors.initials: K
authors.lastname: Heininger
authors.forename: K P
authors.initials: KP
authors.lastname: Schulitz
authors.forename: J
authors.initials: J
authors.lastname: Reinecke
authors.forename: C H
authors.initials: CH
authors.lastname: Evans
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D002417:Cattle; D019054:Evoked Potentials, Motor / Q000502:physiology; D005073:Evoked Potentials, Somatosensory / Q000502:physiology; D005260:Female; D053590:Interleukin 1 Receptor Antagonist Protein; D007375:Interleukin-1 / Q000502:physiology*; D011128:Polyradiculopathy / Q000188:drug therapy* / Q000276:immunology / Q000503:physiopathology; D011239:Prednisolone / Q000627:therapeutic use*; D051381:Rats; D011917:Rats, Inbred Lew; D017472:Receptors, Interleukin-1 / Q000037:antagonists & inhibitors*; D012795:Sialoglycoproteins / Q000627:therapeutic use*; D013126:Spinal Nerve Roots / Q000503:physiopathology*
chemical_list: D000893:Anti-Inflammatory Agents; C507763:IL1RN protein, human; D053590:Interleukin 1 Receptor Antagonist Protein; D007375:Interleukin-1; D017472:Receptors, Interleukin-1; D012795:Sialoglycoproteins; D011239:Prednisolone