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International Journal of Inflammation
Volume 2012, Article ID 810359, 10 pages
Research Article

Resident Corneal Cells Communicate with Neutrophils Leading to the Production of IP-10 during the Primary Inflammatory Response to HSV-1 Infection

1Department of Biology, University of West Georgia, Carrollton, GA 30118, USA
2Department of Microbiology and Immunology, University of South Alabama, Mobile, AL 36688, USA

Received 12 October 2011; Revised 28 November 2011; Accepted 19 December 2011

Academic Editor: Michelle C. Callegan

Copyright © 2012 S. J. Molesworth-Kenyon et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


In this study we show that murine and human neutrophils are capable of secreting IP-10 in response to communication from the HSV-1 infected cornea and that they do so in a time frame associated with the recruitment of CD8+ T cells and CXCR3-expressing cells. Cellular markers were used to establish that neutrophil influx corresponded in time to peak IP-10 production, and cellular depletion confirmed neutrophils to be a significant source of IP-10 during HSV-1 corneal infection in mice. A novel ex vivo model for human corneal tissue infection with HSV-1 was used to confirm that cells resident in the cornea are also capable of stimulating neutrophils to secrete IP-10. Our results support the hypothesis that neutrophils play a key role in T-cell recruitment and control of viral replication during HSV-1 corneal infection through the production of the T-cell recruiting chemokine IP-10.