Serum cytokine profiles in relapsing polychondritis suggest monocyte/macrophage activation.

Published

Journal Article

OBJECTIVE: There is evidence that autoimmunity plays a significant role in the pathogenesis of relapsing polychondritis (RP). This study was designed to investigate circulating levels of various cytokines in relation to the etiology of this rare disorder, and to compare the pattern of cytokine elevations in RP with that in another autoimmune disease, rheumatoid arthritis (RA). METHODS: Serum from 22 patients with active RP and an equal number of age- and sex-matched healthy controls and RA patients were available for analysis. The following cytokines were measured: interleukin-1beta (IL-1beta), IL-2, IL-4, IL-5, IL-6, IL-7, IL-8, IL-10, IL-12, IL-13, IL-17, interferon-gamma (IFNgamma), tumor necrosis factor alpha, granulocyte colony-stimulating factor (G-CSF), granulocyte-macrophage colony-stimulating factor (GM-CSF), monocyte chemoattractant protein 1 (MCP-1), and macrophage inflammatory protein 1beta (MIP-1beta). Results were analyzed by nonparametric Mann-Whitney test with Holm stepdown adjustment for multiple testing. RESULTS: The levels of 3 of these cytokines showed significant differences between RP patients and controls. Compared with controls, mean serum levels of MCP-1, MIP-1beta, and IL-8 were all much higher in patients with active RP. In contrast, RA patients showed a more general increase in all cytokines measured, with much higher levels of IL-2, IL-4, IL-5, IL-6, IL-7, IL-10, IL-13, IFNgamma, G-CSF, GM-CSF, MCP-1, and MIP-1beta compared with controls. CONCLUSION: Levels of 3 serum cytokines were significantly higher in RP patients than in age- and sex-matched controls. One of these 3 cytokines, IL-8, was not significantly elevated in RA samples. Overall, in RP, a more discrete group of cytokines exhibited significantly increased levels than was found in RA. Each of the 3 cytokines that were elevated in RP is a proinflammatory chemokine, characteristic of activation of the monocyte and macrophage lineage, and in the case of IL-8, also of neutrophils. These data suggest a major role for a cell-mediated immune response in the pathophysiology of RP.

Full Text

Duke Authors

Cited Authors

  • Stabler, T; Piette, J-C; Chevalier, X; Marini-Portugal, A; Kraus, VB

Published Date

  • November 2004

Published In

Volume / Issue

  • 50 / 11

Start / End Page

  • 3663 - 3667

PubMed ID

  • 15529362

Pubmed Central ID

  • 15529362

International Standard Serial Number (ISSN)

  • 0004-3591

Digital Object Identifier (DOI)

  • 10.1002/art.20613

Language

  • eng

Conference Location

  • United States