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.
Rothman
Sarah M
SM
Department of Bioengineering, University of Pennsylvania, Philadelphia, Pennsylvania 19104-6321, USA.
Huang
Zhong
Z
Lee
Kathryn E
KE
Weisshaar
Christine L
CL
Winkelstein
Beth A
BA
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