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

R R Rampersad1, D Esserman, M W McGinnis

  • 1Thurston Arthritis Research Center, University of North Carolina School of Medicine, Division of Rheumatology, Allergy, and Immunology, Chapel Hill, NC 27599, USA.

Scandinavian Journal of Rheumatology
|November 20, 2009
PubMed

Insights

S100A8 and S100A9 proteins are not essential for developing inflammatory arthritis in mouse models. Studies using K/BxN serum transfer and collagen-induced arthritis models showed no difference in disease severity without S100A9.

Area of Science:

  • Immunology
  • Rheumatology
  • Molecular Biology

Background:

  • S100A8 and S100A9 are calcium-binding proteins involved in inflammatory diseases.
  • Elevated S100A8/S100A9 levels are observed in autoimmune diseases like rheumatoid arthritis (RA).

Purpose of the Study:

  • To investigate the role of S100A8 and S100A9 in the pathogenesis of inflammatory arthritis.
  • To determine if S100A9 deficiency affects arthritis development in mouse models.

Main Methods:

  • Utilized S100A9 knockout (S100A9 - /-) and wild-type mice.
  • Induced arthritis using K/BxN serum transfer and collagen-induced arthritis (CIA) models.

Main Results:

  • S100A9 - /- mice exhibited similar arthritis severity and histopathology compared to wild-type controls.
  • Defective expression of S100A8 and S100A9 did not alter disease progression in either arthritis model.

Conclusions:

  • S100A8 and S100A9 are not essential for the expression of inflammatory arthritis in the K/BxN serum transfer model.
  • S100A8 and S100A9 are not essential for the expression of inflammatory arthritis in the CIA model.
Abstract

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