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From the Neurobiology Laboratory, Departments of Research and Clinical Neurology, University Hospital, Basel, Switzerland (Drs. Empl, Renaud, Fuhr, Schaeren–Wiemers, and Steck, and B. Erne); and the Department of Neurology (Dr. Straube), Ludwig-Maximilians University, Munich, Germany.
Address correspondence and reprint requests to Dr. Monika Empl, Department of Neurology, Ludwig-Maximilians University, Munich, Marchioninistr. 15, D-81377 Munich, Germany; e-mail: moem{at}brain.nefo.med.uni-muenchen.de
OBJECTIVE: To determine whether the cytokine tumor necrosis factor 
(TNF-) acts as a pain mediator in neuropathic pain in humans.
BACKGROUND: In animal models, inflammatory cytokines such as TNF- have been shown to facilitate neuropathic pain.
METHODS: The expression of TNF- was analyzed immunohistochemically in 20 human nerve biopsy specimens of patients with painful (n = 10) and nonpainful (n = 10) neuropathies. Additionally, serum soluble TNF- 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- showed expression of TNF- in human Schwann cells. Patients with painful neuropathies showed a stronger TNF- 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- 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.
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