Neutralizing KC (CXCL1), but not IL-6 ameliorates recurrent HSK in vivo. (P6340)

• Published in: The Journal of immunology (1950) 2013-05, Vol.190 (1_Supplement), p.182-182.22
• Main Authors: Stuart, Patrick, Yin, Xiao-Tang, Del Rosso, Chelsea, Potter, Chloe, West, Devin
• Format: Article
• Language: English
• ISSN: 0022-1767; 1550-6606
• DOI: 10.4049/jimmunol.190.Supp.182.22

Herpetic stromal keratitis (HSK) is the leading cause of infectious blindness in developed nations and occurs following infection with herpes simplex virus. The mechanism underlying this disease is immune-mediated, involving neutrophils, macrophages, cytokines, and chemokines. We hypothesized that neutralizing the proinflammatory cytokine IL-6 or the chemokine KC (murine CXCL1) would significantly reduce disease in an animal model of HSK. Latently infected mice were reactivated 6 weeks following infection with UV-B light to stimulate recurrent disease. At that time, we administered mAbs against IL-6, KC and control IgG via intraperitoneal injection. We monitored recurrent infection by daily testing tear film for virus for 7 days following reactivation. Corneal disease was evaluated weekly for five weeks. Data shows that neutralizing KC resulted in lower opacity and neovascularization scores for all time points measured when compared to controls. Surprisingly, unlike what is seen in acute HSK, neutralizing IL-6 did not decrease disease. Futhermore, treatment with anti-KC results in significantly less neutrophilic infiltrate of infected corneas. We conclude that CXCL1 and not IL-6 is important in developing recurrent HSK. Furthermore, these results further demonstrate that recurrent and acute HSK share some but not all aspects of disease, and that one common thread is the crucial role that neutrophils play in this potentially blinding disease.