Inflammatory cytokine and chemokine expression is differentially modulated acutely in the dorsal root ganglion in response to different nerve root compressions.

Abstract

Inflammatory proteins were quantified in bilateral dorsal root ganglions (DRGs) at 1 hour and 1 day using a multiplexed assay after 2 different unilateral nerve root compression injuries. To quantify cytokines and a chemokine in the DRG after nerve root compression with and without a chemical injury to determine contributing inflammatory factors in the DRG that may mediate radicular nociception in clinically relevant nerve root pathologies. Inflammatory cytokines are known to relate to the behavioral hypersensitivity induced after injuries to the nerve root. However, the relative expression of these proteins in the DRG after cervical nerve root compression are not known. The right C7 nerve root underwent transient compression (10 gf) or transient compression with a chemical irritation (10 gf + chr). The chemical injury was also given alone (chr), and the nerve root was exposed (sham), providing 2 types of controls. Mechanical allodynia was measured to assess behavioral outcomes. Interleukin (IL)-1b, IL-6, tumor necrosis factor-a, and macrophage inflammatory protein 3 (MIP3) were quantified in bilateral DRGs at 1 hour and 1 day using a multiplexed assay. Ipsilateral allodynia at day 1 after 10 gf + chr was significantly increased over both 10 gf and chr (P < 0.049). Cytokines and MIP3 were not statistically increased over sham at 1 hour. By day 1 after 10 gf + chr, all proteins (IL-1β, IL-6, tumor necrosis factor-a, MIP3) were significantly increased over both normal and sham in the ipsilateral DRG (P < 0.036), and the cytokines were also significantly increased over chr (P < 0.029). Despite allodynia at day 1, cytokines at that time were not increased over normal or sham after either 10 gf or chr. Nerve root compression alone may not be sufficient to induce early increases in proinflammatory cytokines in the DRG after radiculopathy and this early protein response may not be directly responsible for nociception in this type of injury.