Table 2.
TNF-alpha | IFN-alpha | CXCL9 | CXCL10 | |
---|---|---|---|---|
Control + NO donor | 0.71 ± 0.03 | 0.45 ± 0.01 | 0.94 ± 0.02 | 1.27 ± 0.34 |
Control + iNOS inhibitor | 1.01 ± 0.02 | 1.1 ± 0.45 | 0.17 ± 0.04 | 1.1 ± 0.03 |
sFasL | 8.88 ± 1.89† | 4.5 ± 0.7† | 45.2 ± 0.54†† | n.d. |
HSV-1 | 86 ± 9.1†† | 7422 ± 892†† | 152 ± 29†† | 424 ± 39†† |
HSV − 1 + NO donor | 189±35∗∗ | 1247±299∗∗ | 95 ± 23∗ | 146±49∗∗ |
HSV − 1 + iNOS inhibitor | 79 ± 12 | 10401±501∗∗ | 294±51∗∗ | 215±61∗∗ |
HSV − 1 + sFasL | 43 ± 5∗ | 5673 ± 1329 | 445±91∗∗ | 552 ± 59∗∗ |
HSV − 1 + NO donor + sFasL | 49 ± 6.6∗ | 6427 ± 987 | 110 ± 23∗ | 150±45∗∗ |
Cytokine and chemokine expression changes in the mixed glial cultures at 24 h p.i. with HSV-1. Mixed glial cultures were subjected to treatment with the NO donor—SNP (100 μM)—or the inhibitor of iNOS—AMG (50 μM). mRNA levels of IFN-alpha, TNF-alpha, CXCL9, and CXCL10 are shown as expression relative to control on the basis of the 2−∆∆Ct method. mRNA levels were counted from three PCR reactions for each sample. ∗p ≤ 0.05 and ∗∗p ≤ 0.01 versus HSV-1-infected control and †p ≤ 0.05 and ††p ≤ 0.01 versus uninfected control. n.d. means not detected.