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Abstract
Objective: To determine whether the cytokine tumor necrosis factor α (TNF-α) acts as a pain mediator in neuropathic pain in humans.
Background: In animal models, inflammatory cytokines such as TNF-α have been shown to facilitate neuropathic pain.
Methods: The expression of TNF-α was analyzed immunohistochemically in 20 human nerve biopsy specimens of patients with painful (n = 10) and nonpainful (n = 10) neuropathies. Additionally, serum soluble TNF-α receptor I (sTNF-RI) levels were determined in 24 patients with neuropathies, 16 of which were painful and 8 that were painless.
Results: Colocalization studies by confocal fluorescence microscopy for S-100 and TNF-α showed expression of TNF-α in human Schwann cells. Patients with painful neuropathies showed a stronger TNF-α immunoreactivity in myelinating Schwann cells relative to the epineurial background staining compared with patients with nonpainful neuropathy (0.949 ± 0.047 vs 1.010 ± 0.053, p < 0.05). Although there was no difference in sTNF-RI levels between painful (n = 16) and nonpainful (n = 8) neuropathies (sTNF-RI: 1412 ± 545 pg/mL vs 1,318 ± 175 pg/mL), patients with a mechanical allodynia (n = 9) had elevated serum sTNF-RI (1627 ± 645 pg/mL vs 1233 ± 192 pg/mL, p < 0.05) compared with patients without allodynia (n = 15).
Conclusions: TNF-α expression of human Schwann cells may be up-regulated in painful neuropathies. The elevation of sTNF-RI in patients with centrally mediated mechanical allodynia suggests that systemic sTNF-RI levels may influence central pain processing mechanisms.
- Received September 12, 2000.
- Accepted January 30, 2001.
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