Journal of Leukocyte Biology Myeloid cells, immune suppression, tumor immunology
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Published online before print April 23, 2004
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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.0204065

Received for publication February 3, 2004.
Revised March 11, 2004.
Accepted for publication March 13, 2004.

Article

Interleukin-17 regulates expression of the CXC chemokine LIX/CXCL5 in osteoblasts: implications for inflammation and neutrophil recruitment

Matthew J. Ruddy *, Fang Shen {dagger}, Jeffrey B. Smith {ddagger}, Ashu Sharma {dagger}, and Sarah L. Gaffen *{dagger}@

Departments of *Microbiology and Immunology, School of Medicine and Biomedical Sciences, and {dagger}Oral Biology, School of Dental Medicine, University at Buffalo, SUNY, New York; and {ddagger}Division of Neonatology of the Department of Pediatrics, David Geffen School of Medicine and Mattel Children’s Hospital at UCLA, University of California, Los Angeles

@ To whom correspondence should be addressed. E-mail: sgaffen{at}buffalo.edu.


  Abstract

Interleukin (IL)-17 is the founding member of an emerging family of inflammatory cytokines whose functions remain poorly defined. IL-17 has been linked to the pathogenesis of rheumatoid arthritis, and numerous studies implicate this cytokine in inflammation-induced bone loss. It is clear that a major function of IL-17 is to amplify the immune response by triggering production of chemokines, cytokines, and cell-surface markers, ultimately leading to neutrophil chemotaxis and inflammation. As an IL-17 signaling deficiency in mice causes a dramatic reduction in neutrophil chemotaxis and a consequent increased susceptibility to bacterial infection, it is important to define gene targets involved in IL-17-mediated neutrophil trafficking. Here, we demonstrate that IL-17 and tumor necrosis factor {alpha} (TNF-{alpha}) cooperatively induce the lipopolysaccharide-inducible CXC chemokine (LIX; a.k.a., CXC chemokine ligand 5, Scya5, or murine granulocyte chemotactic protein-2) in the preosteoblast cell line MC3T3. LIX is induced rapidly at the mRNA and protein levels, likely through the activation of new gene transcription. Conditioned media from MC3T3 cells treated with IL-17 and/or TNF-{alpha} stimulates neutrophil mobility potently, and LIX is a significant, contributing factor to this process. In addition, IL-17 cooperates with bacterial components involved in periodontal disease to up-regulate LIX expression. This study is the first demonstration of LIX expression in bone cells and has implications for inflammatory bone diseases such as arthritis and periodontal disease.

Key Words: TNF-{alpha} • lipopolysaccharide • GCP-2




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