Journal
NEUROMODULATION
Volume 26, Issue 5, Pages 938-949Publisher
ELSEVIER
DOI: 10.1016/j.neurom.2023.03.006
Keywords
Chemotherapy; chronic pain; non-small cell lung cancer; peripheral neuropathies; spinal cord stimulation
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We conducted a study on the effects of spinal cord stimulation (SCS) on chemoefficacy and chemotherapy-induced peripheral neuropathy (CIPN) pain in rats with xenograft human non-small cell lung cancer. Our findings suggest that preemptive SCS can enhance the antitumor efficacy of paclitaxel (PTX) and prevent PIPN pain by modulating macrophages, fractalkine (CX3CL1), and inflammatory cytokines.
Introduction: Despite increasing utilization of spinal cord stimulation (SCS), its effects on chemoefficacy, cancer progression, and chemotherapy-induced peripheral neuropathy (CIPN) pain remain unclear. Up to 30% of adults who are cancer survivors may suffer from CIPN, and there are currently no effective preventative treatments.Materials and Methods: Through a combination of bioluminescent imaging, behavioral, biochemical, and immunohistochemical approaches, we investigated the role of SCS and paclitaxel (PTX) on tumor growth and PTX-induced peripheral neuropathy (PIPN) pain development in T-cell-deficient male rats (Crl:NIH-Foxn1rnu) with xenograft human non-small cell lung cancer. We hypothesized that SCS can prevent CIPN pain and enhance chemoefficacy partially by modulating macrophages, fractalkine (CX3CL1), and inflammatory cytokines.Results: We show that preemptive SCS enhanced the antitumor efficacy of PTX and prevented PIPN pain. Without SCS, rats with and without tumors developed robust PIPN pain-related mechanical hypersensitivity, but only those with tumors developed cold hypersensitivity, suggesting T-cell dependence for different PIPN pain modalities. SCS increased soluble CX3CL1 and macro-phages and decreased neuronal and nonneuronal insoluble CX3CL1 expression and inflammation in dorsal root ganglia.Conclusion: Collectively, our findings suggest that preemptive SCS is a promising strategy to increase chemoefficacy and prevent PIPN pain via CX3CL1-macrophage modulation.
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