Figure 3From: Defense against HSV-1 in a murine model is mediated by iNOS and orchestrated by the activation of TLR2 and TLR9 in trigeminal ganglia iNOS, gp91, and p22 expression in the trigeminal ganglia of the infected mice and NO production in the infected peritoneal macrophages. Mice were infected intranasally with 106 p.f.u. of HSV-1 and were euthanized 5 days after the infection. The trigeminal ganglia were collected, the RNA extracted, reverse transcribed in cDNA and real-time PCR for the expression of (A) gp91phox, (B) p22phox, and (C) iNOS gene were performed. (D) Macrophages derived from the C57BL/6 mice or the indicated knockout mice were infected with HSV-1 (MOI of 10, five wells/group) (black bars) or were non-infected (NI, white bars), and the levels of nitric oxide (NO) were determined in the supernatants, 24 h after stimulation, by the Griess reaction assay. The bars represent the S.E.M. (*P <0.05, when comparing the infected macrophages to the respective non-infected macrophages; #P <0.05 or ##P <0.01 when comparing the C57BL/6 infected macrophages with the knockout infected macrophages. This experiment is representative of two analyses.Back to article page