Cytokine expression in vivo during murine herpetic stromal keratitis. Effect of protective antibody therapy.

摘要: HSV-1 topical infection on the murine cornea can induce herpetic stromal keratitis (HSK), a T cell-mediated inflammatory response that results in blindness. To begin to decipher molecular interactions involved this infection, extracts of infected corneas were assayed for presence seven different cytokines by ELISA. The most prominent detected IL-1 alpha and IL-6. Both elevated day 2 after reached peak levels 82 538 pg/cornea, respectively, at 10, then diminished over next 10 days. In contrast, TNF-alpha concentrations not seen uninfected any time during 20-day observation period. IFN-gamma granulocyte-macrophage CSF corneal below sensitivity assay. We investigated whether passive transfer antibody viral glycoprotein D, which prevents HSK, influenced production It was found reduced threefold IL-6 undetectable antibody-treated hosts. IL-10 IL-4 control hosts also monitored. Neither these two regulatory associated with HSK development or effective therapy. Naive cultured vitro spontaneously produced IL-6, indicating cells resident had ability synthesize proinflammatory cytokines. Collectively, our imply may be important contributors pathogenesis.