A study published in Molecular Medicine Reports provides further evidence that interleukin (IL)-17 contributes to neuropathic pain through the activation of astrocytes and secretion of proinflammatory cytokines.
In the Molecular Medicine Reports study Caixia Sun and colleagues from the Jiangsu University Zhenjiang, China describe an infiltration with CD4+T cells in the spinal cord in a rat model of post-nerve injury. The authors identified CD4/IL‑17 positive cells located at the superficial laminae of the spinal dorsal horn.
These observations were associated with an up-regulation of IL‑17, IL‑1β and IL‑6 mRNA expression and high IL-17 protein levels in the spinal cord. Importantly, in vitro, IL‑17 stimulated resting astrocytes to produce IL-1β and IL-6 that may be linked to pain hypersensitivity.
The study suggests that IL-17 is involved in local activation of astrocytes and glial response that via the release of pro-inflammatory cytokine drives and maintains neuropathic pain.