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5. TNF and JNK‐mediated inflammatory pain

Author

Bas, DB, Abdelmoaty, S, Sandor, K, Codeluppi, S, Fitzsimmons, B, Steinauer, J, Hua, XY, Yaksh, TL, and Svensson, CI

Subjects
Pain Research, Chronic Pain, Neurosciences, 2.1 Biological and endogenous factors, Aetiology, Neurological, Animals, Astrocytes, Enzyme Activation, Hypersensitivity, Inflammation, JNK Mitogen-Activated Protein Kinases, MAP Kinase Signaling System, Male, Pain, Rats, Sprague-Dawley, Real-Time Polymerase Chain Reaction, Spinal Cord, Tumor Necrosis Factor-alpha, Clinical Sciences, Pharmacology and Pharmaceutical Sciences, Anesthesiology
Abstract

BackgroundMounting evidence points to individual contributions of tumour necrosis factor-alpha (TNF) and the c-Jun N-terminal kinase (JNK) pathway to the induction and maintenance of various pain states. Here we explore the role of spinal TNF and JNK in carrageenan-induced hypersensitivity. As links between TNF and JNK have been demonstrated in vitro, we investigated if TNF regulates spinal JNK activity in vivo.MethodsTNF levels in lumbar cerebrospinal fluid (CSF) were measured by enzyme-linked immunosorbent assay, spinal TNF gene expression by real-time polymerase chain reaction and TNF protein expression, JNK and c-Jun phosphorylation by western blotting. The role of spinal TNF and JNK in inflammation-induced mechanical and thermal hypersensitivity was assessed by injecting the TNF inhibitor etanercept and the JNK inhibitors SP600125 and JIP-1 intrathecally (i.t.). TNF-mediated regulation of JNK activity was examined by assessing the effect of i.t. etanercept on inflammation-induced spinal JNK activity.ResultsTNF levels were increased in CSF and spinal cord following carrageenan-induced inflammation. While JNK phosphorylation followed the same temporal pattern as TNF, c-jun was only activated at later time points. Intrathecal injection of TNF and JNK inhibitors attenuated carrageenan-induced mechanical and thermal hypersensitivity. TNF stimulation induced JNK phosphorylation in cultured spinal astrocytes and blocking the spinal actions of TNF in vivo by i.t. injection of etanercept reduced inflammation-induced spinal JNK activity.ConclusionsHere we show that spinal JNK activity is dependent on TNF and that both TNF and the JNK signalling pathways modulate pain-like behaviour induced by peripheral inflammation.

Published
2015

6. Spinal release of tumour necrosis factor activates c-Jun N-terminal kinase and mediates inflammation-induced hypersensitivity.

Author

Bas, DB, Abdelmoaty, S, Sandor, K, Codeluppi, S, Fitzsimmons, B, Steinauer, J, Hua, XY, Yaksh, TL, and Svensson, CI

Subjects
Spinal Cord, Astrocytes, Animals, Rats, Sprague-Dawley, Pain, Hypersensitivity, Inflammation, JNK Mitogen-Activated Protein Kinases, Tumor Necrosis Factor-alpha, MAP Kinase Signaling System, Enzyme Activation, Male, Real-Time Polymerase Chain Reaction, Rats, Sprague-Dawley, Clinical Sciences, Neurosciences, Pharmacology and Pharmaceutical Sciences, Anesthesiology
Abstract

BackgroundMounting evidence points to individual contributions of tumour necrosis factor-alpha (TNF) and the c-Jun N-terminal kinase (JNK) pathway to the induction and maintenance of various pain states. Here we explore the role of spinal TNF and JNK in carrageenan-induced hypersensitivity. As links between TNF and JNK have been demonstrated in vitro, we investigated if TNF regulates spinal JNK activity in vivo.MethodsTNF levels in lumbar cerebrospinal fluid (CSF) were measured by enzyme-linked immunosorbent assay, spinal TNF gene expression by real-time polymerase chain reaction and TNF protein expression, JNK and c-Jun phosphorylation by western blotting. The role of spinal TNF and JNK in inflammation-induced mechanical and thermal hypersensitivity was assessed by injecting the TNF inhibitor etanercept and the JNK inhibitors SP600125 and JIP-1 intrathecally (i.t.). TNF-mediated regulation of JNK activity was examined by assessing the effect of i.t. etanercept on inflammation-induced spinal JNK activity.ResultsTNF levels were increased in CSF and spinal cord following carrageenan-induced inflammation. While JNK phosphorylation followed the same temporal pattern as TNF, c-jun was only activated at later time points. Intrathecal injection of TNF and JNK inhibitors attenuated carrageenan-induced mechanical and thermal hypersensitivity. TNF stimulation induced JNK phosphorylation in cultured spinal astrocytes and blocking the spinal actions of TNF in vivo by i.t. injection of etanercept reduced inflammation-induced spinal JNK activity.ConclusionsHere we show that spinal JNK activity is dependent on TNF and that both TNF and the JNK signalling pathways modulate pain-like behaviour induced by peripheral inflammation.

Published
2015

11. POSTER ABSTRACTS

Author

Koenemann, K, primary, Steinauer, J, additional, Steele, H, additional, and Turk, J, additional

Published
2021
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34. 1790-1840 : Leçons d'abîme

Author

Fernandes, S. (ed.), Griener, P. (ed.), Reichler, C. (ed.), Schöpfer, H. (ed.), Steinauer, J. (ed.), Reichler, Claude, Fernandes, S. (ed.), Griener, P. (ed.), Reichler, C. (ed.), Schöpfer, H. (ed.), Steinauer, J. (ed.), and Reichler, Claude

Published
2007

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