Cytokine chemokine expression in contused rat spinal cord

Neurochem Int. 2000 Apr;36(4-5):417-25. doi: 10.1016/s0197-0186(99)00133-3.


Spinal cord injury within the first few hours, is complicated by inflammatory mechanisms, including the influx of monocyte/macrophages as well as the activation of resident spinal microglia and astrocytes. Numerous studies have suggested that the initial infiltration of the hematogenous cells may be due to the secretion of cytokines and chemokines in the injured CNS. In order to elucidate which chemotactic factors may be expressed following traumatic spinal cord contusion, the presence of mRNA for a number of cytokines, chemokines and growth factors was examined in contused rat spinal cord by reverse transcriptase-polymerase chain reaction and immunohistochemistry. Spinal injury was accompanied by an increase in glial fibrillary acidic protein mRNA suggesting astrocyte activation and astrogliosis. TNFalpha message levels were upregulated as early as 1 h post injury and returned to baseline levels by 3 days post injury (DPI). By immunocytochemistry, staining for TNFalpha increased at 1 and 3 dpi and was predominantly diffuse in the necrotic tissue. The chemokines IP-10, MCP-1, and MIP-1alpha were also detected in the injured spinal cord. mRNA levels of IP-10 peaked around 6 h post injury and were upregulated up to 7 dpi. MCP-1 mRNA was detected at 1 h post injury and its levels returned to baseline by 14 dpi. An increase in MCP-1 staining was observed from 1 to 7 dpi. The staining was also diffuse in the necrotic tissue and also localized to cells near the site of injury. The presence of aFGF and bFGF was also detected in the injured spinal cord. mRNA for aFGF was detected at 0 time, increased at 6 h post injury, peaked at 3 days, and remained elevated up to 21 days. bFGF mRNA was initially detected at 1 h post injury, increased between 6 h and 3 days, declined thereafter and returned to baseline levels by 21 days.

MeSH terms

  • Animals
  • Chemokines / genetics
  • Chemokines / metabolism*
  • Contusions / metabolism*
  • Contusions / pathology
  • Cytokines / genetics
  • Cytokines / metabolism*
  • Immunohistochemistry
  • Macrophages / pathology
  • Male
  • Microglia / pathology
  • RNA, Messenger / metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Reverse Transcriptase Polymerase Chain Reaction
  • Spinal Cord Diseases / metabolism*
  • Spinal Cord Diseases / pathology


  • Chemokines
  • Cytokines
  • RNA, Messenger