Satellite glial cells synthesize IL-6 and express signal-transducing receptors to mediate IL-6 effect in the rat neuropathic pain model
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| Year of publication | 2009 |
| Type | Conference abstract |
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| Description | Many experimental studies have documented important role of cytokines during different types of neuropathy and their potential to induce or facilitate neuropathic pain. Interleukin-6 (IL-6) is a proinflammatory cytokine involved as a key signal molecule in the neuronal and immune responses to nerve injury. A biological effect of IL-6 is mediated by two signal-transducing receptors: glycoprotein 130 (gp130) and IL-6 receptor (IL6r). The gp130 receptor is a transmembrane glycoprotein and integral part of STAT3 signaling pathway. We have investigated immunohistochemical localization of IL-6, gp130, IL6r and activated STAT3 in both ipsilateral and contralateral lumbar (L4-5) and cervical (C7-8) dorsal root ganglia (DRG) following chronic constriction injury (CCI) of sciatic nerve. Immunostaining for glutamine synthetase (GS) and ED-1 were used for detection of satellite glial cells (SGC) and macrophages, respectively. In addition, in situ hybridization was used to prove IL-6 synthesis in DRG. Twenty eight male rats were operated on triple unilateral ligation of right sciatic nerve (CCI) and allowed to survive for 1, 3, 7 and 14 days. All surgical procedures were performed aseptically under deep anesthesia by a xylazine and ketamine. To test neuropathic pain induction, withdrawal threshold of mechanoallodynia and thermal hyperalgesia was measured by Dynamic plantar aesthesiometer (UGO BASILE) and Plantar test (UGO BASILE), respectively. Immunohistochemical and in situ hybridization results revealed that besides neurons SGC of DRG associated with injured nerve are source of IL-6 protein. Bilateral elevation of immunostaining for IL-6r in SGC was detected only in L4-5 DRG 1 week from CCI. In contrast to naive DRG, enhanced immunoreactivity for gp130 and STAT3 was present in SGC of both C7-8 and L4-5 DRG following unilateral CCI. The results suggest that unilateral nerve injury used as neuropathic pain model induces synthesis of IL-6 and its IL-6r in the SGC of DRG associated with injured nerve. Therefore, biological effects of IL-6 during neuropathic pain are probably driven by IL-6r, because gp130 and activated STAT3 are expressed by SGC of both cervical and lumbal segments. |
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