Skip to main content
. 2021 Jan 19;131(2):e142468. doi: 10.1172/JCI142468

Figure 3. TREM-1 pharmacologic stimulation worsens angiotensin-II–induced AAA.

Figure 3

(A) Apoe–/– mice were implanted with subcutaneous osmotic minipumps infusing AngII (1000 ng/kg/min), and were injected intraperitoneally with an agonist TREM-1 monoclonal antibody (TREM-1 Ab) or isotype control (isotype Ab) (200 μg/kg/d), every day for 3 or 7 days. (B) Quantification of IL-1β, TNF-α, and IL-6 production (ELISA) by LPS/INF-γ–stimulated splenocytes. (C) Quantification of sTREM-1 plasma levels at day 3 following AngII infusion and TREM-1 Ab or isotype Ab treatment (n = 9/group). (D) Quantitative analysis and representative photomicrographs of the maximal abdominal aortic diameter at day 28 (n = 12 in the isotype Ab group, n = 10 in TREM-1 Ab group). (E) AAA incidence at day 28. Scale bars: 1 mm. (F) Quantification and representative photomicrographs of the number of elastin layers in the aortic wall after Orcein staining at day 7 (n = 5/group). Scale bars: 50 μm. (G) Quantification of Il1b, Tnfa, Mmp2, and Mmp9 mRNA expression in aorta at day 7 by RT-qPCR (n = 7 in the isotype Ab group, n = 12 in TREM-1 Ab group). (H) Flow cytometry quantification and representative dot plots of Ly6Chi classical monocyte number into the aortic wall and (I) in the blood (n = 12 in the isotype Ab group and n = 10 in the TREM-1 Ab group). Results are displayed as the mean ± SEM. *P < 0.05, **P < 0.01, ****P < 0.0001, by Mann-Whitney test.