Previous research confirmed gut dysbiosis and translocation of selected intestinal bacteria into the vessel wall in abdominal aortic aneurysm patients. We studied the stool, blood, thrombus and aneurysm microbiomes of 21 abdominal aortic aneurysm patients using 16S rRNA sequencing. Our goals were to determine: 1. whether the microbiome characteristic of an aneurysm differs from that of a healthy vessel, 2. whether bacteria detectable in the aneurysm are translocated from the gut through the bloodstream, 3. whether the enzymatic activity of the aneurysm microbiome can contribute to the destruction of the vessel wall. The abundance of Acinetobacter, Burkholderia, Escherichia, and Sphingobium in the aneurysm samples was significantly higher than that in the microbiome of healthy vessels, but only a part of these bacteria can come from the intestine via the blood. Environmental bacteria due to the oral cavity or skin penetration route, such as Acinetobacter, Sphingobium, Enhydrobacter, and Aquabacterium, were present in the thrombus and aneurysm with a significantly higher abundance compared to the blood. Among the enzymes of the microbiome associated with the healthy vessel wall, Iron-chelate-transporting ATPase and Polar-amino-acid-transporting ATPase have protective effects. In addition, bacterial Peptidylprolyl isomerase activity found in the aneurysm has an aggravating effect on the formation of aneurysm.

Operating under septic conditions poses significant challenges in vascular surgery. Infection is a serious risk when handling synthetic vessel prostheses and is one of the most dreaded complications. In the event of graft infection, an infection-resistant alternative is necessary. Cryopreserved vascular allografts offer a suitable alternative to replace an infected vessel or a section of a synthetic graft. However, there are no international guidelines for the preparation, storage, and thawing of such vessel grafts. Here, we aimed to investigate the mechanical properties of human cryopreserved arteries across multiple scales, ranging from nanonewton to newton forces and identify the optimal cryogenic storage duration. Human arterial allograft samples were frozen in a slow, controlled process and stored at −80 °C. One native and four cryopreserved samples were examined during a six-month-long period. Dimethyl-sulphoxide was used as a cryoprotectant. The mechanical properties of fresh and stored samples were explored in uniaxial ring tests and nanoindentation. We found no significant changes in the multi-scale mechanical properties during the examination period. Our results indicate that the cryopreserved vascular allografts are mechanically stable for up to six months under cryogenic conditions; hence, they represent ideal samples in vascular surgery.

Abdominal aortic aneurysm (AAA) is a life-threatening vascular condition characterized by inflammatory degeneration of the vessel wall. Emerging evidence suggests that microbial factors contribute to its progression. In this study, we analyzed the mycobiome composition of stool, blood, thrombus and damaged vessel wall samples collected during surgery from 24 AAA patients using Internal Transcribed Spacer (ITS) sequencing. Significant differences in alpha and beta diversity were observed across the sample types, confirming compartmentalization of the mycobiome. However, individual fungal profiles did not establish a clear gut-blood-vessel wall axis, indicating that fungi translocated to the vessel wall may originate from other anatomical regions. Comparison AAA mycobiome with healthy arterial walls’ mycobiome from organ donors revealed a dominance of anti-inflammatory Tomentella in healthy samples, while pro-inflammatory Malassezia species were prevalent in damaged vessel walls. These findings highlight the role of fungi in AAA progression and suggest potential thera-peutic avenues, including antifungal adjuvant treatments to mitigate inflammation and aneurysm development.

Abdominal aortic aneurysm (AAA) is a lethal vascular disease characterized by intramural hemorrhage. This study delineates the signatures of heme and its metabolic imbalance related to progression and inflammation in AAA. Clinical analyses of patients undergoing open AAA surgery show that AAA patients exhibit vascular inflammation, with elevated serum CRP, IL-6, and heme levels correlating with the expression of heme-regulated gene Hmox1/HO-1 (heme oxygenase-1) in the affected aortic wall. Oxidation of hemoglobin to ferri state leading to accumulation of methemoglobin readily releasing heme occurs in human AAA and in angiotensin II (AngII)-induced AAA in apolipoprotein E-deficient mice. Transcriptomic analysis for AngII-induced AAA identifies upregulated genes predominantly enriched in inflammatory signaling, extracellular matrix degradation, oxidative stress pathways, and altered expression of genes related to heme metabolism including Hmox1. Immunohistochemistry for IL1β and TNFα confirms inflammatory activation within AAA tissues. The signatures of heme-responsive gene inductions, enhanced expression of HO-1 and H-ferritin, are detected. Mechanistic studies employing endothelial cells and smooth muscle cells reveal that heme exposure of resident cells markedly enhances the expression of IL1β and ICAM1, as well as the inflammasome component NLRP3, and such inflammatory response is controlled by HO-1. Intervention with Normosang (heme arginate), an HO-1 inducer, attenuates aneurysm progression, whereas HO-1 inhibition by Tin protoporphyrin IX abolishes this protection. Induction of HO-1 accompanied by elevated H-ferritin level also mitigated aortic wall inflammation as reflected by lowering IL1β and TNFα. These findings highlight the heme-HO-1-H-ferritin axis as an element of AAA pathogenesis and a potential therapeutic target.