Cytokine mRNA expression in painful radiculopathy.
Inflammatory cytokines contribute to lumbar radiculopathy. Regulation of cytokines for transient cervical injuries, with or without longer-lasting inflammation, remains to be defined. The C7 root in the rat underwent compression (10gf), chromic gut suture exposure (chr), or their combination (10gf+chr). Ipsilateral C7 spinal cord and dorsal root ganglia (DRG) were harvested at 1 hour after injury for real-time PCR analysis of IL-1beta, IL-6, and TNF-alpha. Cytokine mRNA increased after all 3 injuries. TNF-alpha mRNA in the DRG was significantly increased over sham after 10gf+chr (P = .026). Spinal IL-1beta was significantly increased over sham after 10gf and 10gf+chr (P < .024); IL-6 was significantly increased after 10gf+chr (P < .024). In separate studies, the soluble TNF-alpha receptor was administered at injury and again at 6 hours in all injury paradigms. Allodynia was assessed and tissue samples were harvested for cytokine PCR. Allodynia significantly decreased with receptor administration for 10gf and 10gf+chr (P < .005). Treatment also significantly decreased IL-1beta and TNF-alpha mRNA in the DRG for 10gf+chr (P < .028) at day 1. Results indicate an acute, robust cytokine response in cervical nerve root injury with varying patterns, dependent on injury type, and that early increases in TNF-alpha mRNA in the DRG may drive pain-related signaling for transient cervical injuries.


CONCLUSIONS
Inflammatory cytokine mRNA in the DRG and spinal cord are defined after painful cervical nerve root injury. Studies describe a role for TNF-alpha in mediating behavioral sensitivity and inflammatory cytokines in transient painful radiculopathy. Results outline an early response of inflammatory cytokine upregulation in cervical pain.
Department of Bioengineering, University of Pennsylvania, Philadelphia, Pennsylvania 19104-6321, USA.
Sarah M
SM
Rothman
Zhong
Z
Huang
Kathryn E
KE
Lee
Christine L
CL
Weisshaar
Beth A
BA
Winkelstein
D000818:Animals; D016207:Cytokines / Q000235:genetics*; D004195:Disease Models, Animal; D005727:Ganglia, Spinal / Q000378:metabolism; D015870:Gene Expression / Q000187:drug effects; D053583:Interleukin-1beta / Q000235:genetics; D015850:Interleukin-6 / Q000235:genetics; D008297:Male; D009408:Nerve Compression Syndromes / Q000150:complications / Q000503:physiopathology; D010146:Pain / Q000209:etiology / Q000503:physiopathology; D010147:Pain Measurement / Q000379:methods; D010812:Physical Stimulation / Q000379:methods; D012333:RNA, Messenger / Q000235:genetics* / Q000378:metabolism; D011843:Radiculopathy / Q000209:etiology / Q000235:genetics* / Q000503:physiopathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D047888:Receptors, Tumor Necrosis Factor, Type I / Q000008:administration & dosage; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013116:Spinal Cord / Q000378:metabolism; D013126:Spinal Nerve Roots / Q000293:injuries / Q000503:physiopathology; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics; D015854:Up-Regulation / Q000187:drug effects / Q000235:genetics
D016207:Cytokines; D053583:Interleukin-1beta; D015850:Interleukin-6; D012333:RNA, Messenger; D047888:Receptors, Tumor Necrosis Factor, Type I; D014409:Tumor Necrosis Factor-alpha