4.7 Article

Association of Aneurysm Tissue Neutrophil Mediator Levels with Intraluminal Thrombus Thickness in Patients with Abdominal Aortic Aneurysm

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BIOMOLECULES
卷 12, 期 2, 页码 -

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MDPI
DOI: 10.3390/biom12020254

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abdominal aortic aneurysm; intraluminal thrombus; neutrophil mediators

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This study compared the levels of inflammatory mediators in different thicknesses of intraluminal thrombus (ILT) and adjacent abdominal aortic aneurysm (AAA) walls. The results showed that neutrophil elastase, TNF-a, and IL-6 levels were significantly higher in thick ILT and aneurysmal walls covered by thick ILT. Positive correlations were also found between thick ILT and the adjacent wall, as well as thin ILT and the adjacent wall. These findings suggest that neutrophil mediators and inflammatory cytokines may accumulate differently in AAA tissues based on ILT thickness, potentially weakening the AAA wall.
An intraluminal thrombus (ILT), which accumulates large numbers of neutrophils, plays a key role in abdominal aortic aneurysm (AAA) pathogenesis. This study aimed to compare levels of selected neutrophil inflammatory mediators in thick and thin ILT, plus adjacent AAA walls, to determine whether levels depend on ILT thickness. Neutrophil mediator levels were analysed by enzyme-linked immunosorbent assays in thick and thin segments of ILT, plus adjacent aneurysm wall sections, taken from one aneurysm sac each from 36 AAA patients. In aneurysmal walls covered by thick ILT, neutrophil elastase and TNF-a levels were significantly higher, as were concentrations of IL-6, in thick ILT compared to thin layers. Positive correlations of NGAL, MPO, and neutrophil elastase were observed between thick ILT and the adjacent wall and thin ILT and the adjacent wall, suggesting that these mediators probably infiltrate thick AAA compartments as well as thin. These observations might support the idea that neutrophil mediators and inflammatory cytokines differentially accumulate in AAA tissues according to ILT thickness. The increased levels of neutrophil mediators within thicker AAA segments might suggest the existence of an intensified proinflammatory state that in turn presumably might preferentially weaken the AAA wall at that region.

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