Plasma cytokine levels and risks of abdominal aortic aneurysms: A population-based prospective cohort study

Abstract

Background Abdominal aortic aneurysm (AAA) is characterized by inflammatory cell accumulation in AAA lesions that produce inflammatory cytokines and advance its pathogenesis. Peripheral cytokines may predict the degree or risk of AAA. Methods and Results ELISA determined plasma interleukin-6 (IL6), IL10, IL17A, IFN-γ, and C-reactive protein (CRP) from 476 AAA patients and 200 controls. AAA patients had lower IL6, IFN-γ, IL10, IL17A, and higher CRP than controls. IL10 correlated positively with IFN-γ, IL17A, or IL6, but not CRP in control or AAA populations. IL10 associated negatively with systolic blood pressure, whereas CRP associated positively with diastolic blood pressure and body mass index. CRP was an independent AAA risk factor and correlated positively with aortic diameters before and after adjustments for other risk factors. IFN-γ, IL17A, and CRP correlated positively with cross-sectional AAA area after adjustment. IL10 correlated positively with AAA growth rate before and after adjustment. AAA patients with CRP levels above the median doubled the risk of death. Conclusions Reduced IFN-γ, IL10, and IL17A in AAA patients, positive correlations of IFN-γ and IL17A with cross-sectional AAA area, IL10 with AAA growth rate, and IL10 with IFN-γ and IL17A suggest combined Th1, Th2, and Th17 immune responses in human AAAs.

Association of ficolin‐3 with abdominal aortic aneurysm presence and progression

“…A positive association of these two parameters was observed (Spearman 0 s rho, 0.25; P < 0.001), after adjustment for potential confounding factors (Table 3). Similarly, CRP correlated with aortic diameter, as previously reported [15]. Cox regression analyses of the association of ficolin-3 levels above and below the median and the need for later preventive repair showed a significant increased risk if the ficolin-3 level was above the median, which was after adjustment for potential confounding factors (adjusted hazard ratio, 1.55; 95% CI, 1.11, 2.15)] ( Table 4).…”

Association Between Diverticular Disease and Abdominal Aortic Aneurysms: Pooled Analysis of Two Population Based Screening Cohorts

“…The observation that other chronic inflammatory conditions, for example rheumatoid arthritis, 22 are also associated with a higher prevalence of AAA, supports a direct effect of inflammation on aortic wall integrity, and prospective observational studies have found plasma cytokine levels (interleukins and C-reactive protein) to be significantly associated with aneurysm growth rates. 23,24 This may also indicate that diverticular inflammation contributes to the initiation of AAA, albeit the temporal relationship between diverticular disease and AAA could not be reliably determined in the present study. The finding of a median time interval of 9.3 years from a first diagnosis of diverticular disease to the screening date for patients with AAA and a median age of 63.9 years at diverticular diagnosis make it most likely that diverticular disease precedes AAA in the majority of cases.…”

Atherosclerotic Descending Aortic Aneurysms. Pros and Cons of Surgery

“…Interactions between autoantibodies and antigen-specific Т-lymphocytes, and corresponding aortic wall antigens induce immunoinflammatory response in vascular walls attended by migration, adhesion and infiltration of all layers of aorta with neutrophiles, monocytes/macrophages [19] [20], dendritic and mast cells [21], and В-and Т-lymphocytes [22] [23]. Activation signals (microbial products, immune complexes, proinflammatory cytokines, and bioactive complement protein fragments) produced on cell components result in the activation, synthesis and secretion of a broad number of molecular products including free radicals, cytokines, metalloprotease, chymase, and cytokines [24] [25]. It results in a dramatic inflammatory intensification, impaired structural and functional aortic integrity, accompanied by enlarged aortic fragment.…”