Figure 3.

Schematic of indirect damage to AAA caused by inflammatory response to the gut-aortic axis. Bacteroides fragilis PSA has been shown to impact Th1/Th2 ratio. NLRP3 inflammasomes, members of the NOD-like receptor (NLRs) family, are widely present in vascular endothelial cells and various immune cells. Activation of TLR and NLRP3 inflammasomes during initial immunity can exacerbate vascular wall damage through caspase-mediated apoptosis. MCs, MΦ, and NEU are activated by LPS and then release a variety of pro-inflammatory factors. EOS upregulation of IL4 regulates the polarization of MΦ and monocytes and blocks NF-κB activation in aortic inflammation and vascular wall cells. Notably, IL-6 can chemotact monocytes/macrophages and activate STAT3 and MCP-1 to promote the expansion of the abdominal aorta. Various inflammatory factors and enzymes lead to the formation, growth and rupture of AAA. PSA, polysaccharide A; NLR, NOD-like receptor; TLRs, toll-like receptors.