Fig. 7: Pharmacological blockade of Trem1 using mLR12 decreases the aortic rupture rate.

a Trem1 was highly expressed in the macrophage subpopulation. b Schematic illustration of the treatment procedure. Two biological replicates (n = 8 for each replicate) were performed for each group. All measurements were performed after 28 days of treatment. c Survival curves of mice treated with mLR12 or vehicle (saline solution). d Summary of the normal, TAAD, and rupture rates in each group. e mLR12 treatment could significantly decrease the aortic rupture rate. f Quantification of plasma levels of sTREM1. n = 6 for each group. g Quantification of the mRNA expression of Tnfa, Il1b, Il6, Trem1, and Cd11b in the aorta by qPCR (n = 3). h Immunofluorescence staining for Cd11b⁺Trem1⁺ cells in mouse aorta of the mLR12 treatment group. i Immunofluorescence staining for Cd11b⁺Trem1⁺ cells in mouse aorta of the BAPN + vehicle group. j The percentage of the Cd11b⁺Trem1⁺ cells in each sample was calculated based on the immunofluorescence staining. Wilcoxon rank-sum test, P = 0.0004. n = 9 for each group. k Immunofluorescence staining for CD11b⁺TREM1⁺ cells in aortic adventitia of human TAAD patients. l Immunofluorescence staining for CD11b⁺TREM1⁺ cells in aortic adventitia of healthy donors. m The expression of TREM1 in aortic tissues of human TAAD patients (n = 8) and healthy donors (n = 6) measured by bulk RNA-seq. n The expression of TREM1 in CD11b⁺ and CD11b⁻ cells sorted from the aortic tissues of TAAD patients (n = 4) measured by bulk RNA-seq. In f and g, all values are means ± SEM. *P < 0.05, **P < 0.01, n.s. not significant, Kruskal–Wallis test followed by multiple pairwise comparisons between groups.