The Potential Role of the Gut-Vascular Axis in Ciprofloxacin-Associated Aggravation of Aortic Dissection.

Ciprofloxacin (CIP) is associated with an increased risk of aortic dissection (AD); however, the underlying mechanism remains unclear. This study investigates the potential contribution of gut microbiota and intestinal barrier alterations to CIP-associated AD progression. The AD model was established using a combination of β-aminopropionitrile and angiotensin II. The composition of the gut microbiota was analyzed using 16 S rRNA sequencing. In vivo experiments were conducted to investigate whether CIP aggravates AD through a potential gut-vascular axis involving intestinal alterations and increased circulating lipopolysaccharide (LPS) levels, which was further explored in human aortic smooth muscle cells (HASMCs). The results showed that CIP aggravated aortic injury and induced smooth muscle cell dysfunction in AD mice. CIP disrupted gut microbial composition and impaired intestinal barrier integrity, which was accompanied by increased circulating LPS levels. Additionally, in vitro experiments demonstrated that combined CIP and LPS stimulation enhanced HASMC apoptosis and phenotypic switching. Our findings suggest that CIP-associated intestinal alterations and elevated circulating LPS levels may contribute to AD progression through a potential gut-vascular axis, providing new insights into fluoroquinolone-associated vascular injury and potential gut-targeted interventions.