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Rheumatology Advance Access published online on June 17, 2008
Rheumatology, doi:10.1093/rheumatology/ken185
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© The Author 2008. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Characterization of the immune response in the synovitis, acne, pustulosis, hyperostosis, osteitis (SAPHO) syndrome

M. Hurtado-Nedelec1,2, S. Chollet-Martin1,2, P. Nicaise-Roland1, S. Grootenboer-Mignot1, R. Ruimy3, O. Meyer4 and G. Hayem4

1Immunology, Auto-immunity and Hypersensibility Unit, AP-HP Bichat Claude Bernard Hospital, Paris, 2Univ Paris-Sud 11, INSERM, Châtenay-Malabry, 3Department of Microbiology and 4Department of Rheumatology, AP-HP Bichat Claude Bernard Hospital, Paris, France.

Correspondence to: G. Hayem, Service de Rhumatologie, Hôpital Bichat, 46 rue Henri Huchard, 75018 Paris, France. E-mail: gilles.hayem{at}bch.ap-hop-paris.fr; gilles.hayem{at}bch.aphp.fr


  Abstract

Objective. The aetiology of SAPHO (synovitis, acne, palmoplantar pustulosis, hyperostosis, osteitis) syndrome seems to involve genetic, infectious and immunological components. We examined innate and adaptive immune responses in SAPHO syndrome, as compared with PsA and RA. We also studied the effect of etanercept on immunological parameters.

Methods. We studied 29 patients with SAPHO syndrome, as well as 22 patients with RA, 21 patients with PsA and 15 healthy controls. Adaptive immune responses were investigated by assaying total serum immunoglobulins and several autoantibodies. Innate immunity was studied by quantifying blood PMN functions and plasma cytokine levels. PMN responses to Propionibacterium acnes were tested ex vivo. Eight patients who received etanercept for refractory rheumatic disorders were tested before and after 28 days of treatment.

Results. SAPHO syndrome was associated with elevated IL-8 and IL-18 plasma levels. IL-8 and TNF-{alpha} production by purified PMN was higher in the three patient groups than in the healthy controls, but the oxidative burst and IL-18 production were normal. No autoantibodies were detected in SAPHO patients. Induction of PMN IL-8 and TNF-{alpha} production by P. acnes was impaired in the SAPHO group as compared with the RA and PsA groups. After 28 days of etanercept therapy, PMN IL-8 and TNF-{alpha} production was down-regulated and TNF-{alpha} plasma levels were increased.

Conclusions. These results support the view that the SAPHO syndrome may be triggered by an infectious state involving P. acnes, contributing to the strong humoral and cellular pro-inflammatory responses. Etanercept modulation of PMN activation status emphasizes these new immunological findings.

KEY WORDS: SAPHO syndrome, Innate immunity, Tumour necrosis factor-{alpha}, Polymorphonuclear neutrophil, Propionibacterium acnes, Interleukin-8

Submitted 23 October 2007; revised version accepted 10 April 2008.
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