Granulocyte-macrophage colony-stimulating factor is a key mediator in experimental osteoarthritis pain and disease development View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2012-10

AUTHORS

Andrew D Cook, Jarrad Pobjoy, Stefan Steidl, Manuela Dürr, Emma L Braine, Amanda L Turner, Derek C Lacey, John A Hamilton

ABSTRACT

INTRODUCTION: Granulocyte-macrophage colony-stimulating factor (GM-CSF) has been shown to be important in the development of inflammatory models of rheumatoid arthritis and there is encouraging data that its blockade may have clinical relevance in patients with rheumatoid arthritis. The aims of the current study were to determine whether GM-CSF may also be important for disease and pain development in a model of osteoarthritis. METHODS: The role of GM-CSF was investigated using the collagenase-induced instability model of osteoarthritis. We studied both GM-CSF-/- mice and wild-type (C57BL/6) mice treated prophylactically or therapeutically with a monoclonal antibody to GM-CSF. Disease development (both early and late) was evaluated by histology and knee pain development was measured by assessment of weight distribution. RESULTS: In the absence of GM-CSF, there was less synovitis and matrix metalloproteinase-mediated neoepitope expression at week 2 post disease induction, and less cartilage damage at week 6. GM-CSF was absolutely required for pain development. Therapeutic neutralization of GM-CSF not only abolished the pain within 3 days but also led to significantly reduced cartilage damage. CONCLUSIONS: GM-CSF is key to the development of experimental osteoarthritis and its associated pain. Importantly, GM-CSF neutralization by a therapeutic monoclonal antibody-based protocol rapidly and completely abolished existing arthritic pain and suppressed the degree of arthritis development. Our results suggest that it would be worth exploring the importance of GM-CSF for pain and disease in other osteoarthritis models and perhaps clinically for this form of arthritis. More... »

PAGES

r199

Identifiers

URI

http://scigraph.springernature.com/pub.10.1186/ar4037

DOI

http://dx.doi.org/10.1186/ar4037

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1021994978

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/22995428


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