Open Access Research article

Serum COMP-C3b complexes in rheumatic diseases and relation to anti-TNF-α treatment

Kaisa E Happonen1, Tore Saxne2, Pierre Geborek2, Maria Andersson3, Anders A Bengtsson2, Roger Hesselstrand2, Dick Heinegård4 and Anna M Blom1*

Author affiliations

1 Department of Laboratory Medicine Malmö, Section of Medical Protein Chemistry, Lund University, Wallenberg Laboratory floor 4, SE-205 02 Malmö, Sweden

2 Department of Clinical Sciences Lund, Section of Rheumatology, Lund University, Kioskgatan 3, SE-221 85 Lund, Sweden

3 R and D Centre, Spenshult Hospital for Rheumatic Diseases, SE-313 92 Oskarström, Sweden

4 Department of Clinical Sciences Lund, Section of Rheumatology, Lund University, BMC C12, SE-221 84 Lund, Sweden

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Citation and License

Arthritis Research & Therapy 2012, 14:R15  doi:10.1186/ar3694

Published: 20 January 2012

Abstract

Introduction

Cartilage oligomeric matrix protein (COMP) is found at elevated concentrations in sera of patients with joint diseases such as rheumatoid arthritis (RA) and osteoarthritis (OA). We recently showed that COMP activates complement via the alternative pathway and that COMP-C3b complexes are present in sera of RA patients, but not in healthy controls. We now set out to elaborate on the information provided by this marker in a variety of diseases and larger patient cohorts.

Methods

COMP-C3b levels in sera were measured by using an enzyme-linked immunosorbent assay (ELISA) capturing COMP and detecting C3b. Serum COMP was measured by using ELISA.

Results

COMP-C3b levels were significantly elevated in patients with RA as well as in systemic lupus erythematosus (SLE), compared with healthy controls. SLE patients with arthritis had significantly higher COMP-C3b levels than did those without. COMP-C3b was furthermore elevated in patients with ankylosing spondylitis (AS), psoriatic arthritis (PsA), reactive arthritis, systemic sclerosis, and OA. COMP-C3b did not correlate with COMP in any of the patient groups. COMP-C3b correlated with disease activity in RA, but not in other diseases. COMP-C3b levels in RA patients decreased on treatment with tumor necrosis factor (TNF)-α inhibitors, whereas the levels increased in patients with AS or PsA. The changes of COMP-C3b did not parallel the changes of C-reactive protein (CRP).

Conclusions

COMP-C3b levels are elevated in several rheumatologic diseases and correlate with inflammatory measures in RA. COMP-C3b levels in RA decrease during TNF-α inhibition differently from those of CRP, suggesting that formation of COMP-C3b relates to disease features not reflected by general inflammation measures.