title: Increased interleukin-1α and prostaglandin E2 expression in the spinal cord at 1 day after painful facet joint injury: evidence of early spinal inflammation.
abstract: METHODS
  This study used immunohistochemistry and an enzyme immunoassay to quantify interleukin-1α (IL-1α) and prostaglandin E2 (PGE2) levels in the spinal cord of rats at 1 day after painful cervical facet joint injury.
  
  
  OBJECTIVE
  The objective of this study was to determine to what extent spinal inflammation is initiated early after a painful loading-induced injury of the C6-C7 facet joint in a rat model.
  
  
  BACKGROUND
  A common source of neck pain, the cervical facet joint is susceptible to loading-induced injury, which can lead to persistent pain. IL-1α and PGE2 are associated with joint inflammation and pain, both locally in the joint and centrally in the spinal cord. Joint inflammation has been shown to contribute to pain after facet joint injury. Although spinal neuronal hyperactivity is evident within 1 day of painful facet injury, it is unknown if inflammatory mediators, such as IL-1α and PGE2, are also induced early after painful injury.
  
  
  METHODS
  Rats underwent either a painful C6-C7 facet joint distraction or sham procedure. Mechanical sensitivity was assessed, and immunohistochemical and enzyme immunoassay techniques were used to quantify IL-1α and PGE2 expression in the spinal cord at day 1.
  
  
  RESULTS
  Both IL-1α and PGE2 were significantly elevated (P≤ 0.04) at day 1 after painful injury. Moreover, although both spinal IL-1α and PGE2 levels were correlated with the withdrawal threshold in response to mechanical stimulation of the forepaw, this correlation was only significant (P = 0.01) for PGE2.
  
  
  CONCLUSIONS
  The increased expression of 2 inflammatory markers in the spinal cord at 1 day after painful joint injury suggests that spinal inflammation may contribute to the initiation of pain after cervical facet joint injury. Further studies will help identify functional roles of both spinal IL-1α and PGE2 in loading-induced joint pain.
  
  
  METHODS
  N/A.
authors.affiliation: Departments of *Bioengineering and †Neurosurgery, University of Pennsylvania, Philadelphia, PA.
authors.forename: Jeffrey V
authors.initials: JV
authors.lastname: Kras
authors.forename: Ling
authors.initials: L
authors.lastname: Dong
authors.forename: Beth A
authors.initials: BA
authors.lastname: Winkelstein
mesh_terms: D000818:Animals; D002574:Cervical Vertebrae / Q000293:injuries* / Q000378:metabolism; D015232:Dinoprostone / Q000096:biosynthesis* / Q000235:genetics; D005786:Gene Expression Regulation; D053582:Interleukin-1alpha / Q000096:biosynthesis*; D008297:Male; D009187:Myelitis / Q000378:metabolism / Q000473:pathology*; D010146:Pain / Q000378:metabolism / Q000473:pathology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D018078:Receptors, Prostaglandin E / Q000096:biosynthesis / Q000235:genetics; D013116:Spinal Cord / Q000378:metabolism / Q000473:pathology; D013997:Time Factors; D021801:Zygapophyseal Joint / Q000293:injuries*
chemical_list: D053582:Interleukin-1alpha; D018078:Receptors, Prostaglandin E; D015232:Dinoprostone