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Scandinavian Journal of Rheumatology Volume 38, 2009 - Issue 6
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Articles

S100A9 is not essential for disease expression in an acute (K/BxN) or chronic (CIA) model of inflammatory arthritis

RR Rampersad Thurston Arthritis Research Center, University of North Carolina School of Medicine, Division of Rheumatology, Allergy, and Immunology, Chapel Hill, NC
,
D Esserman University of North Carolina School of Medicine, Division of General Medicine and Clinical Epidemiology, Chapel Hill, NC
,
MW McGinnis Thurston Arthritis Research Center, University of North Carolina School of Medicine, Division of Rheumatology, Allergy, and Immunology, Chapel Hill, NC
,
DM Lee Division of Rheumatology, Allergy, and Immunology, Brigham and Women's Hospital, Boston, MA, USA
,
DD Patel Thurston Arthritis Research Center, University of North Carolina School of Medicine, Division of Rheumatology, Allergy, and Immunology, Chapel Hill, NC; Novartis Institutes for BioMedical Research, Basel, Switzerland
&
TK Tarrant Thurston Arthritis Research Center, University of North Carolina School of Medicine, Division of Rheumatology, Allergy, and Immunology, Chapel Hill, NCCorrespondence[email protected]
Pages 445-449 | Published online: 18 Nov 2009
 
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Abstract

Objective: S100A8 (calgranulin A, MRP8) and S100A9 (calgranulin B, MRP14) are calcium-binding proteins highly expressed by activated myeloid cells and thought to be involved in the pathogenesis of inflammatory diseases. Circulating levels of S100A8/S100A9 are elevated in both human and experimental models of autoimmune disease, including rheumatoid arthritis (RA).

Methods: Mice deficient in S100A9 (S100A9 − /−) and wild-type controls were immunized using standard techniques for the K/BxN serum transfer or the collagen-induced arthritis (CIA) model.

Results: S100A9 − /− animals, with defective expression of both S100A8 and S100A9 proteins, had similar arthritis and histopathology to that of wild-type controls in both mouse models.

Conclusion: S100A8 and S100A9 are not essential for disease expression in either the K/BxN serum transfer or the CIA model of inflammatory arthritis.

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