Figure 4.

IL-17A deficiency blunted inflammatory response and aortic dissections. Age matched WT and IL-17A−/− mice were treated with Sham or Ang II for 14 d. During Ang II treatment, in vivo imaging of aortas was performed with ultrasonography and diameters of aortas were measured (A). Percentage of aortic dissection featured by presence of intramural hematomas was recorded (left panel). White bars: animals treated with Ang II for 7 d. Black bars: animals treated with Ang II for 14 d. n=12 in each group. Right panel: aortic diameters were recorded at 6 and 12 d for each treatment group. Circles: sham-treated mice, n=5 mice respectively for WT and IL-17A−/−. Squares: Ang II-treated mice, n=6 for WT mice and n=9 for IL-17A−/− mice. *, p<0.05; ns, no significance. (B) Flow cytometric analysis of aortic CD4-positive and IL-17A-positive cells was performed and number of double-positive cells was measured. n=4 in each group. (C) MCP-1 was measured in aortic explant culture medium. White bars: sham-treated WT; Black bars Ang II-treated WT; Grey bars: Ang II-treated IL-17A−/−. n=5–6 in each group. *, p<0.05. (D) Flow cytometric analysis of CD11b-positive macrophages in dissociated aortic cells was performed. A representative measurement is shown. Grey curves: Sham-treated WT at 7 d. Red curves: Ang II-treated WT at 7 d. Blue curves: Ang II-treated IL-17−/− at 7d. n=2 in each group. (E) Systolic blood pressure was measured via a non-invasive tail-cuff method in conscious WT (> 4 months old) and IL-17−/− mice (> 8 months old) at baseline and at d 7 of Ang II infusion, as indicated. *, p<0.05.