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MARIA I. BOKAREWA, TAO JIN, and ANDREJ TARKOWSKI

ABSTRACT.

Objective. Defensins and bactericidal/permeability-increasing protein (BPI) are the components of the azurophilic granules of polymorphonuclear cells (PMNC) maintaining antimicrobial protection. Both these substances have been suggested to interact with the host immune system rather than merely kill invading pathogens. We assessed concentrations of BPI and a-defensins in synovial fluid (SF) and matching blood samples of patients with rheumatoid arthritis (RA).

Methods. Matching samples of SF and blood were collected from 67 patients with RA (aged 21–73 yrs) with acute joint effusion. Blood samples from 22 healthy individuals made up a control group. Concentrations of BPI and human neutrophil peptides (HNP 1–3) were measured by ELISA. The results were related to radiological signs of destructive arthritis, duration of the disease, and laboratory markers of inflammation.

Results. BPI and HNP concentrations in SF were 10–60 times higher than in matching blood samples (p < 0.0001). Strong correlations between BPI and HNP concentrations were found in both blood and SF. In SF, BPI and HNP concentrations correlated to white blood cell (WBC) count (p < 0.001), and were associated with erosive joint disease (p < 0.05). In contrast, WBC count, serum C-reactive protein, or rheumatoid factor were not significantly correlated to the BPI or HNP concentrations. Serum BPI concentrations were moderately but significantly increased in RA patients compared in blood to controls (p < 0.05).

Conclusion. BPI and HNP are accumulated in the synovial cavity of patients with RA. Significant correlation between joint erosion and local occurrence of BPI and HNP suggests participation of these molecules in regulation of the destructive course of RA. (J Rheumatol 2003;30:1719-24)

Key Indexing Terms:

ARTHRITIS
INFLAMMATION
DEFENSINS

Supported by the Göteborg Medical Society, Swedish Association Against Rheumatism, King Gustaf V Foundation, Swedish Medical Research Council, Nanna Svartz Foundation, Börje Dahlin Foundation, National Inflammation Network, and the University of Göteborg.

M.I. Bokarewa, MD, PhD; T. Jin, MD; A. Tarkowski, MD, PhD.

Address reprint requests to Dr. M. Bokarewa, Department of Rheumatology and Inflammation Research, Gulhedsgatan 10, S-413 46 Göteborg, Sweden. E-mail: maria.bokarewa@rheuma.gu.se

Submitted June 14, 2002; revision accepted January 30, 2003.