Open AccessAbsence of a classically activated macrophage cytokine signature in peripheral spondylarthritis, including psoriatic arthritis
Author(s) -
Vandooren Bernard,
Noordenbos Troy,
Ambarus Carmen,
Krausz Sarah,
Cantaert Tineke,
Yeremenko Nataliya,
Boumans Maartje,
Lutter Rene,
Tak Paul P.,
Baeten Dominique
Publication year - 2009
Publication title -
arthritis & rheumatism
Language(s) - English
Resource type - Journals
eISSN - 1529-0131
pISSN - 0004-3591
DOI - 10.1002/art.24406
Subject(s) - medicine , synovitis , psoriatic arthritis , cd163 , rheumatoid arthritis , immunology , cytokine , tumor necrosis factor alpha , arthritis , synovial fluid , inflammation , macrophage , reactive arthritis , macrophage polarization , pathology , in vitro , osteoarthritis , biology , biochemistry , alternative medicine
Objective Peripheral spondylarthritis (SpA) is characterized by macrophages that express CD163, a marker of alternative activation (M2). The purpose of this study was to assess whether this differential infiltration with macrophage subsets was associated with a different local inflammatory milieu in SpA as compared with rheumatoid arthritis (RA). Methods The effect of SpA and RA synovial fluid (SF) on macrophage polarization was tested in vitro on normal peripheral blood monocytes. SF levels of classically activated macrophage (M1)–derived and alternatively activated macrophage (M2)–derived mediators were analyzed by enzyme‐linked immunosorbent assay and multiparameter Luminex bead assay in 47 patients with non‐psoriatic SpA, 55 with RA, and 15 with psoriatic arthritis (PsA). Paired synovial biopsy samples were analyzed histologically. Results SF from SpA patients promoted preferential expression of the M2 markers CD163 and CD200R in vitro, even if SF levels of the prototypical M2‐polarizing factors (interleukin‐4 [IL‐4], IL‐13, and IL‐10) were not increased as compared with those in RA SF. Despite a similar degree of overall joint inflammation in SpA and RA, SpA synovitis displayed strongly reduced SF levels of M1‐derived, but not M2‐derived, mediators, such as tumor necrosis factor α (TNFα), IL‐1β, IL‐12p70, and interferon‐γ–inducible protein 10. SF levels of M1‐derived mediators correlated well with peripheral joint inflammation in RA, but neither these mediators nor IL‐1α and IL‐17 did so in SpA. Of interest, the SF cytokine profile in PsA, a more destructive subtype of SpA, was similar to that in non‐psoriatic SpA. Conclusion The local inflammatory milieu is clearly different in SpA as compared with RA peripheral arthritis. Synovitis in SpA, including that in PsA, is characterized by a selective decrease in M1‐derived proinflammatory mediators, such as TNFα and IL‐1β.