Abstract

Objectives: The goal of this study was to determine if highly collagenolytic bacteria introduced to the gut microbiome induces abdominal aortic aneurysm in mice. Methods: C57BL/6 mice received a prolonged 4-day course of preoperative antibiotics (oral clindamycin and subcutaneous cefoxitin) and received pre- and postoperative enemas containing either 10% glycerol solution (control) or a freshly prepared bacterial suspension with a highly collagenolytic strain of Serratia marcescens (S2). All mice underwent laparotomy, aortic crush injury with forceps, and application of either 0.9% sodium chloride (control) or 10% calcium chloride to the periadventitial aortic space. Aortic diameter was measured on initial exposure and on sacrifice on postoperative day 21. Groups were compared using a series of Student’s T-test. Results: On postoperative day 21, the difference in aortic diameter for mice treated with periadventitial sodium chloride and glycerol enema was minimal (control 1, n=6, 0.03 mm ± 0.30). In mice treated with periadventitial calcium chloride and glycerol enema, fusiform aneurysm was reliably produced compared to control 1 (control 2, n=6, 0.53 mm ± 0.30, p ≤ 0.05). In mice treated with periadventitial sodium chloride and S2 enema, fusiform aneurysm was reliably produced with a significant difference in diameter compared to control 1 (n=8, 0.63 mm ± 0.30, p ≤ 0.05). In mice treated with periadventitial calcium chloride and S2 enema, fusiform aneurysm was reliably produced with a significant difference in diameter compared to control 1 (n=8, 0.59 mm ± 0.30, p ≤ 0.05). There was no significant difference between the 2 treatment groups. Conclusions: The introduction of highly collagenolytic Serratia marcescens to the gut microbiome of mice in addition to aortic crush injury reliably produces fusiform aortic aneurysm in this model. Further investigation is required to elucidate the mechanism of aneurysm formation.

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