Plasma concentrations of interleukin-6, C-reactive protein, tumor necrosis factor-α and matrix metalloproteinase-9 in aortic dissection

Wen, Dan; Zhou, Xin; Li, Jianjun; Luo, Fang; Zhang, Lin; Gao, Linggen; Wang, Linping; Song, Lei; Sun, Kai; Zou, Yubao; Zhang, Channa; Hui, Rutai

doi:10.1016/j.cca.2011.09.029

Cited by 63 publications

(58 citation statements)

References 21 publications

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“…This condition may determine the reduction of perfusion of numerous organs with devastating complications (1-3). Recent evidence suggests inflammation as the principal mechanism of aorta AD medial degeneration (6,(9)(10)(11)(12). In particular, it has been demonstrated that inflammatory cells, such as lymphocytes and macrophages, not only increase the expression of proteases and cell adhesion molecules, but also release reactive oxygen species.…”

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confidence: 99%

“…In particular, it has been demonstrated that inflammatory cells, such as lymphocytes and macrophages, not only increase the expression of proteases and cell adhesion molecules, but also release reactive oxygen species. Thus, they contribute to the apoptosis of vascular smooth muscle cells (VSMCs) in the aortic artery, and finally lead to medial degradation (6,(9)(10)(11)(12). Furthermore, this condition determines increases in systemic inflammatory molecules [i.e.…”

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confidence: 99%

“…Furthermore, this condition determines increases in systemic inflammatory molecules [i.e. Interleukin-6 (lL-6) and tumor necrosis factor-a (TNF-a), metalloproteinase (MMP)s, C-reactive protein (CRP)], as detected in individuals with aortic dissection (6,(9)(10)(11)(12).…”

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confidence: 99%

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The Role of Inflammation in Type a Aortic Dissection: A Pilot Study

et al. 2013

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Type A aortic dissection (TAAD) is a severe cardiovascular disease with high mortality rates. Current evidence suggests inflammation as the main mechanism of its complex pathophysiology. Accordingly, in this study the eventual presence of inflammatory cells in aorta specimens and any contribution of these cells in both apoptosis and metalloproteinase levels were assessed. The potential relationship between plasma inflammatory molecules and TAAD was also detected. In addition, implication in TAAD susceptibility of ten common and functional single nucleotide polymorphisms (SNP)s of six candidate genes (CCR5, TLR4, ACE, eNOs, MMP-9 and -2) was determined. Thus, histo-pathological and immunoistochemical aorta examination, TUNEL testing, genotyping of ten SNPs were performed. Levels of plasma inflammatory molecules were also determined using ELISA technique. A significant inflammatory infiltrate was observed in the examined aortas. Consistent with these data, significantly higher plasma levels of systemic inflammatory mediators characterized the cases. In addition, a high risk genotype significantly associated with TAAD susceptibility was identified. Thus, inflammation producing MMPs, cytokines and death mediators seem to be the shared pathological mechanism for TAAD in the population examined.

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The Role of Inflammation in Type a Aortic Dissection: A Pilot Study

et al. 2013

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“…Further confirming our results, the expression of MMP-12 has been reported within aortic specimens [9,10] both in humans and in mice [11], and it has been specifically related to the pathogenesis of aneurysms occurring both in ascending and in abdominal aortas [12,13]. This is different from what occurs with MMP-2 and MMP-9, which are released by several immune cells and have been related to matrix remodeling also in atherosclerotic plaque [14,15,16,17]. …”

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confidence: 42%

MMP-12 and Macrophage Activation in Acute Aortic Dissection

Porto

Cifani²,

Proietta³

et al. 2014

Cardiology

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“…During the activation of the extrinsic pathway, protease-activated receptor in the cell membrane of injured tissue is activated, resulting in the release of inflammatory cytokines such as tumor necrosis factor-α, and interleukins-1β and -6, which are other potential causes of a fever (20). Indeed, the plasma concentrations of interleukin-6 causing CRP production in the liver are reportedly elevated in AAD (21).…”

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A Fever in Acute Aortic Dissection is Caused by Endogenous Mediators that Influence the Extrinsic Coagulation Pathway and Do Not Elevate Procalcitonin

et al. 2016

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Objective A fever is observed in approximately one-third of cases of acute aortic dissection (AAD); however, the causes remain unclear. We investigated the mechanism of a fever in AAD by measuring the serum concentrations of inflammatory markers, mediators of coagulation and fibrinolysis, and procalcitonin, a marker of bacterial infection. Methods We retrospectively studied 43 patients with medically treated AAD without apparent infection. Patients were divided into those with (Group A; n=19) and without (Group B; n=24) a maximum body temperature >38 . We established which patients fulfilled the criteria for systemic inflammatory response syndrome (SIRS), and its relationship with a fever was examined. Mediators of inflammation, coagulation and fibrinolysis were compared by a univariate analysis. Factors independently associated with a fever were established by a multivariate analysis. Results The criteria for SIRS were fulfilled in a greater proportion of patients in Group A (79%) than in Group B (42%, p=0.001). There was no difference in the procalcitonin concentration between Groups A and B (0.15 0.17 ng/mL vs. 0.11 0.12 ng/mL, respectively; p=0.572). Serum procalcitonin concentrations lay within the normal range in all patients in whom it was measured, which showed that the fever was caused by endogenous mediators. On the multivariate analysis, there was a borderline significant relationship between a fever and the prothrombin time-International Normalized Ratio (p=0.065), likely reflecting the extrinsic pathway activity initiated by tissue factor. Conclusion Our findings suggest that a fever in AAD could be caused by SIRS, provoked by endogenous mediators that influence the extrinsic coagulation pathway without elevating the serum procalcitonin concentration.

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Plasma concentrations of interleukin-6, C-reactive protein, tumor necrosis factor-α and matrix metalloproteinase-9 in aortic dissection

Cited by 63 publications

References 21 publications

The Role of Inflammation in Type a Aortic Dissection: A Pilot Study

The Role of Inflammation in Type a Aortic Dissection: A Pilot Study

MMP-12 and Macrophage Activation in Acute Aortic Dissection

A Fever in Acute Aortic Dissection is Caused by Endogenous Mediators that Influence the Extrinsic Coagulation Pathway and Do Not Elevate Procalcitonin

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