Blocking of cytokines signalling attenuates evoked and spontaneous neuropathic pain behaviours in the paclitaxel rat model of chemotherapy ‐induced neuropathy

ConclusionsThe findings support the notion that cytokines/chemokines, particularly TNF‐α, IL‐1 and MCP‐1, are involved in the pathophysiology of CIPNP and suggest that strategies that target their inhibition may be effective in treating CIPNP. SignificanceThis study demonstrates that paclitaxel‐treated rats exhibit, in addition to indices of mechanical and cold hypersensitivity, a behavioural sign of spontaneous pain, the principal compliant of patients with neuropathic pain. This was accompanied by upregulation in plasma levels of key cytokines/chemokines (IL‐1α, IL‐1β, IL‐6, TNF‐α, INF‐γ and MCP‐1) 31 days post‐treatment. However, it is noteworthy that cytokine release, rather than nerve injury per se, may be causative of NP in this model of CIPNP. Nevertheless, our findings that pharmacological blockade of TNF‐α, IL‐1β and MCP‐1 attenuated both evoked and spontaneous pain suggest that strategies that target inhibition of these cytokines may be effective in treating CIPNP.
Source: European Journal of Pain - Category: Anesthesiology Authors: Tags: Original Article Source Type: research