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A more recent version of this article appeared on February 1, 2008

Published online before print November 12, 2007
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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.0807571

Received for publication August 24, 2007.
Revised October 18, 2007.
Accepted for publication October 19, 2007.

Article

IL-17 receptor signaling influences virus-induced corneal inflammation

Sara J. Molesworth-Kenyon , Rong Yin , John E. Oakes , and Robert N. Lausch @

Department of Microbiology and Immunology, College of Medicine, University of South Alabama, Mobile, Alabama, USA

@ To whom correspondence should be addressed. E-mail: rlausch{at}jaguar1.usouthal.edu.


  Abstract

IL-17 has been associated with selected inflammatory and autoimmune diseases. We characterized the expression of this proinflammatory cytokine following HSV-1 corneal infection and investigated whether IL-17R signaling modulated the host response to the viral pathogen at early time-points postinfection. IL-17 was elevated in the murine cornea 24 h after high-dose virus infection and subsequently persisted at low levels during the first week. Immunofluorescent studies showed that the IL-17R was expressed by cultured mouse corneal fibroblasts. Exposure of corneal cells to IL-17 led to production of IL-6 and MIP-2 in vitro and in vivo, indicating that the IL-17R was functional. Mice lacking IL-17R displayed significantly reduced neutrophil infiltration and corneal opacity. However, this effect was transient, as corneal pathology and neutrophil influx resembled that of wild-type (WT) hosts 4 days postinfection. HSV-1 growth and clearance in IL-17R-/- hosts were similar to that of the WT controls. Infection of IFN-{gamma} gene knockout mice was associated with elevated IL-17 levels and accelerated corneal opacity, suggesting that IFN-{gamma} negatively regulated IL-17 expression. Collectively, our results establish that IL-17 is rapidly produced in the cornea after HSV-1 infection and is regulated at least in part by IFN-{gamma}. The absence of IL-17 signaling results in a transient decrease in the expression of proinflammatory mediators, neutrophil migration, and corneal pathology, but control of virus growth in the cornea and trigeminal ganglia is not compromised. Thus, IL-17 actively influences early virus-induced corneal inflammation.

Key Words: HSV-1 • neutrophil • IFN-{gamma}




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