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Rheumatology Advance Access originally published online on April 8, 2008
Rheumatology 2008 47(6):809-814; doi:10.1093/rheumatology/ken056
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© The Author 2008. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Investigation of the role of IL-1 and TNF in matrix degradation in the intervertebral disc

J. A. Hoyland, C. Le Maitre and A. J. Freemont

Tissue Injury and Repair Group, Research School of Clinical and Laboratory Sciences, The University of Manchester, Manchester, UK.

Correspondence to: A. J. Freemont, Tissue Injury and Repair Group, Research School in Clinical and Laboratory Sciences, Stopford Building, The University of Manchester, Oxford Road, Manchester M13 9PT, UK. E-mail: tony.freemont{at}manchester.ac.uk


  Abstract

Objective. To establish if IL-1 or TNF regulates matrix degradation in the non-degenerate or degenerate intervertebral disc (IVD).

Methods. In situ zymography (ISZ) has been used to investigate the role of IL-1 and TNF in the matrix degradation characterizing symptomatic IVD degeneration. ISZ employed three substrates (gelatin, collagen II, casein) and four different challenges, IL-1β, IL-1 receptor antagonist (IL-1Ra), TNF-{alpha} and anti-TNF.

Results. We have shown for the first time that whilst IL-1β will stimulate and IL-1 receptor antagonist will inhibit matrix degradation in intact human IVD tissue, neither TNF-{alpha} nor anti-TNF have any measurable effect on degradation of these matrices.

Conclusion. This study has addressed a current area of controversy in IVD biology, namely, whether either IL-1 or TNF or both are involved in driving matrix degradation. Our data indicate that IL-1 is a key cytokine mediating matrix degradation in the IVD and therefore a therapeutic target.

KEY WORDS: Intervertebral disc, Interleukin-1, Interleukin-1Ra, Tumour necrosis factor, In situ zymography, Matrix degradation

Submitted 6 August 2007; revised version accepted 24 January 2008.
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A. J. Freemont
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