Peri-sciatic proinflammatory cytokines, reactive oxygen species, and complement induce mirror-image neuropathic pain in rats
| Autor: | Carin M. Twining, Stephen Poole, Evan M. Sloane, Steven F. Maier, David Martin, Marucia Chacur, Henry Marsh, Linda R. Watkins, Erin D. Milligan |
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| Rok vydání: | 2003 |
| Předmět: |
Male
Sciatic Neuropathy Sialoglycoproteins Inflammation Antibodies Functional Laterality Receptors Tumor Necrosis Factor Proinflammatory cytokine Rats Sprague-Dawley chemistry.chemical_compound Physical Stimulation medicine Animals Drug Interactions Pain Measurement Behavior Animal Dose-Response Relationship Drug business.industry Interleukin-6 Superoxide Dismutase Zymosan Complement System Proteins medicine.disease Catalase Sciatic Nerve Complement system Rats Receptors Complement Disease Models Animal Interleukin 1 Receptor Antagonist Protein Tumor Necrosis Factor Decoy Receptors Anesthesiology and Pain Medicine Peripheral neuropathy Neurology chemistry Hyperalgesia Receptors Tumor Necrosis Factor Type I Immunology Cytokines Neuralgia Tumor necrosis factor alpha Neurology (clinical) medicine.symptom business Carrier Proteins Reactive Oxygen Species |
| Zdroj: | Pain. 110(1-2) |
| ISSN: | 0304-3959 |
| Popis: | In inflammatory neuropathy, immune activation near intact peripheral nerves induces mechanical allodynia. The identity of the peripheral immune product(s) that lead to these changes in pain behavior is unknown. The present series of studies utilized the sciatic inflammatory neuropathy (SIN) model to examine this question. Here, inflammatory neuropathy is created by injecting an immune activator (zymosan) around one sciatic nerve via an indwelling catheter. Our prior studies demonstrated that peri-sciatic zymosan activated macrophages and neutrophils to release proinflammatory cytokines and reactive oxygen species (ROS). In addition, zymosan is a classical activator of the complement cascade. Thus the present series of experiments examined whether any of these inflammatory mediators are involved in the initial induction of SIN-induced ipsilateral or bilateral allodynias. Peri-sciatic injection of selective inhibitors/antagonists revealed that a number of immune products are early mediators of the resultant allodynias, including proinflammatory cytokines (tumor necrosis factor, interleukin-1, and interleukin-6), ROS, and complement. Thus these immune-derived substances can markedly alter sensory nerve function at mid-axon. |
| Databáze: | OpenAIRE |
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