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Absence of a classically activated macrophage cytokine signature in peripheral spondylarthritis, including psoriatic arthritis.

AbstractOBJECTIVE:
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 alpha (TNFalpha), IL-1beta, IL-12p70, and interferon-gamma-inducible protein 10. SF levels of M1-derived mediators correlated well with peripheral joint inflammation in RA, but neither these mediators nor IL-1alpha 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 TNFalpha and IL-1beta.
AuthorsBernard Vandooren, Troy Noordenbos, Carmen Ambarus, Sarah Krausz, Tineke Cantaert, Nataliya Yeremenko, Maartje Boumans, Rene Lutter, Paul P Tak, Dominique Baeten
JournalArthritis and rheumatism (Arthritis Rheum) Vol. 60 Issue 4 Pg. 966-75 (Apr 2009) ISSN: 0004-3591 [Print] United States
PMID19333931 (Publication Type: Comparative Study, Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Biomarkers
  • Cytokines
Topics
  • Adult
  • Aged
  • Arthritis, Psoriatic (immunology, pathology)
  • Arthritis, Rheumatoid (immunology, pathology)
  • Biomarkers (metabolism)
  • Biopsy
  • Cytokines (immunology, metabolism)
  • Female
  • Humans
  • Macrophages (immunology, metabolism, pathology)
  • Male
  • Middle Aged
  • Spondylarthritis (immunology, pathology)
  • Synovial Membrane (immunology, pathology)

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