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The Journal of Immunology, 2001, 167: 2879-2886.
Copyright © 2001 by The American Association of Immunologists

A Role for IL-18 in Neutrophil Activation1

Bernard P. Leung2,*, Shauna Culshaw2,*, J. Alastair Gracie{dagger}, David Hunter*, Claudio A. Canetti{ddagger}, Carol Campbell*, Fernando Cunha{ddagger}, Foo Y. Liew* and Iain B. McInnes3,{dagger}

* Departments of Immunology and Bacteriology, Western Infirmary, and {dagger} Centre for Rheumatic Diseases, Royal Infirmary, University of Glasgow, Glasgow, United Kingdom; and {ddagger} Department of Pharmacology, School of Medicine Ribeirao Preto, University of Sao Paulo, Sao Paulo, Brazil

IL-18 expression and functional activity has been identified in several autoimmune and infectious diseases. To clarify the potential role of IL-18 during early innate immune responses, we have explored the capacity of IL-18 to activate neutrophils. Human peripheral blood-derived neutrophils constitutively expressed IL-18R ({alpha} and {beta}) commensurate with the capacity to rapidly respond to IL-18. IL-18 induced cytokine and chemokine release from neutrophils that was protein synthesis dependent, up-regulated CD11b expression, induced granule release, and enhanced the respiratory burst following exposure to fMLP, but had no effect upon the rate of neutrophil apoptosis. The capacity to release cytokine and chemokine was significantly enhanced in neutrophils derived from rheumatoid arthritis synovial fluid, indicating differential responsiveness to IL-18 dependent upon prior neutrophil activation in vivo. Finally, IL-18 administration promoted neutrophil accumulation in vivo, whereas IL-18 neutralization suppressed the severity of footpad inflammation following carrageenan injection. The latter was accompanied by reduction in tissue myeloperoxidase expression and suppressed local TNF-{alpha} production. Together, these data define a novel role for IL-18 in activating neutrophils and thereby promoting early innate immune responses.




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