Skip to main content
. Author manuscript; available in PMC: 2015 Oct 15.
Published in final edited form as: J Immunol. 2014 Sep 8;193(8):4095–4106. doi: 10.4049/jimmunol.1401192

Figure 6. IL-1 signaling is critical for regulating CXCL12 expression in the CNS during WNV infection.

Figure 6

Assessment of homeostatic chemokine expression in the CNS. Following cardiac perfusion, brain tissue was harvested and analyzed from WNV-infected WT (closed squares) and IL-1R1−/− mice (open squares) at indicated time points for CXCL12α/β (A), CXCR4, and CXCR7 (E) mRNA via qRT-PCR, normalized to GAPDH, and are presented as the mean fold change in mRNA levels over uninfected controls. Statistical significance of increased or decreased chemokine expression in WNV-infected IL-1R1−/− mice was determined in comparison with infected WT mice. Data are averages of results for at least 4 mice and reflect at least two independent experiments. (B) Confocal analysis of CXCL12β (red) and CD31 (green) expression from brainstem region of WNV-infected WT (left) and IL-1R1−/− mice (right) collected on day 8 p.i. (C) Quantitative analysis of CXCL12β expression in both WT and IL-1R1−/− mice brain tissue. Representative images are shown from 3 experiments in which 8-10 images were analyzed from 4-5 mice per group. *p<0.05, **p<0.01, ***p<0.001