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.
Astrocytes are the most abundant glial cells in the central nervous system (CNS), and were historically regarded as support cells. Evidence has demonstrated that astrocytes are important for maintenance of neuropathic pain. In all models of neuropathic pain, such as rhizotomy, chronic constriction injury and spinal nerve ligation, proliferation and activation of astrocytes has been demonstrated, and inhibiting astrocytes in the spinal cord was demonstrated to reduce neuropathic pain. However, the activation of astrocytes and how they mediate neuropathic pain requires further elucidation.
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.
The study determined that IL-17 increases in the ipsilateral spinal cord dorsal horn at day 7 post-SNL and observed IL-17 is located in CD4+ cells via double immunostaining.
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.
In conclusion, the study demonstrated that IL-17 is involved in maintaining neuropathic pain. Elevated IL-17 may be produced by infiltrated CD4+T cells.