Pro and Anti‐Inflammatory Cytokine Networks in Atherosclerosis

Autieri, Michael V.

doi:10.1002/9781118828533.ch26

Cited by 6 publications

(9 citation statements)

References 52 publications

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“…This complex milieu consists of multiple cytokines with redundant, pleiotropic, and opposing effects, and the balance of pro- and anti-inflammatory cytokines often determines plaque severity and stability. Cells present in the lesion must interrogate and respond to this multitude of factors in an appropriate fashion, which together often result in the development and progression of atherosclerosis [34, 35]. The inflammatory process in the atherosclerotic artery may lead to increased blood levels of inflammatory cytokines and other acute-phase reactants [36].…”

Section: Discussionmentioning

confidence: 99%

Evaluation of the Effect of Andrographolide on Atherosclerotic Rabbits Induced byPorphyromonas gingivalis

Batran

Al-Bayaty

Al-Obaidi

et al. 2014

BioMed Research International

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Epidemiologic evidence has demonstrated significant associations between atherosclerosis and Porphyromonas gingivalis (Pg). We had investigated the effect of andrographolide (AND) on atherosclerosis induced by Pg in rabbits. For experimental purpose, we separated thirty male white New Zealand rabbits into 5 groups. Group 1 received standard food pellets; Groups 2–5 were orally challenged with Pg; Group 3 received atorvastatin (AV, 5 mg/kg), and Groups 4-5 received 10 and 20 mg/kg of AND, respectively, over 12 weeks. Groups treated with AND showed significant decrease in TC, TG, and LDL levels (P < 0.05) and significant increase in HDL level in the serum of rabbits. Furthermore, the treated groups (G3–G5) exhibited reductions in interleukins (IL-1β and IL-6) and C-reactive protein (CRP) as compared to atherogenicgroup (G2). The histological results showed that the thickening of atherosclerotic plaques were less significant in treated groups (G3–G5) compared with atherogenicgroup (G2). Also, alpha-smooth muscle actin (α-SMA) staining decreased within the plaques of atherogenicgroup (G2), while it was increased in treated groups (G3–G5). Lastly, groups treated with AV and AND (G3–G5) showed significant reduction of CD36 expression (P < 0.05) compared to atherogenicgroup (G2). These results substantially proved that AND contain antiatherogenic activity.

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Section: Discussionmentioning

confidence: 99%

Evaluation of the Effect of Andrographolide on Atherosclerotic Rabbits Induced byPorphyromonas gingivalis

Batran

Al-Bayaty

Al-Obaidi

et al. 2014

BioMed Research International

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“…Deposition of cholesterol (primarily packaged in low density lipoproteins (LDL)) at these sites drives the accumulation of monocyte-derived macrophages in an attempt to clear the lipid deposits. This lipid-driven inflammatory response drives the formation of a microenvironment rich in oxidized LDL (oxLDL), cytokines, growth factors, and wound-associated extracellular matrix proteins (fibronectin, osteopontin) [1–4] (Figure 1). These stimuli induce vascular smooth muscle cells in the media to lose their contractile properties, attain a synthetic, fibroproliferative phenotype, and migrate into the vessel intima [5].…”

Section: A Introductionmentioning

confidence: 99%

Integrin signaling in atherosclerosis

Finney

Stokes

Pattillo

et al. 2017

Cell. Mol. Life Sci.

109

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Atherosclerosis, a chronic lipid-driven inflammatory disease affecting large arteries, represents the primary cause of cardiovascular disease in the world. The local remodeling of the vessel intima during atherosclerosis involves the modulation of vascular cell phenotype, alteration of cell migration and proliferation, and propagation of local extracellular matrix remodeling. All of these responses represent targets of the integrin family of cell adhesion receptors. As such, alterations in integrin signaling affect multiple aspects of atherosclerosis, from the earliest induction of inflammation to the development of advanced fibrotic plaques. Integrin signaling has been shown to regulate endothelial phenotype, facilitate leukocyte homing, affect leukocyte function, and drive smooth muscle fibroproliferative remodeling. In addition, integrin signaling in platelets contributes to the thrombotic complications that typically drive the clinical manifestation of cardiovascular disease. In this review, we examine the current literature on integrin regulation of atherosclerotic plaque development and the suitability of integrins as potential therapeutic targets to limit cardiovascular disease and its complications.

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“…on the coronary endothelium [18]. TNF-α is a proinflammatory cytokine that impact on endothelial dysfunction, contributes to plaque rupture and adhesion molecule expression blood coagulation [8]. TNFα is a powerful inducer of local inflammation.…”

Section: Immunological Examinationmentioning

confidence: 99%

“…Once being inside the vascular tissue, C. pneumoniae has been shown to act directly on the cells involved in atherosclerotic process, contributing to endothelial dysfunction, foam cell formation, vascular smooth muscle cell (VSMC) proliferation and migration, and platelet aggregation and induce the elicitation of proinflammatory cytokines like TNF-α, and adhesion molecules, such as ICAM-1 thus contributing to the chronic inflammatory state responsible for the initiation, progression, and destabilisation of atherosclerotic plaque [4,7].TNF-α is a proinflammatory cytokine with a diversity of biological actions, displayed essential effects on various cell forms that are constituents of atherosclerotic lesions. Each of endothelial cells, macrophages, and smooth muscle cells can produce TNF [8]. High level of TNF-α was linked with the pathogenesis of several situations like myocardial dysfunction and CAD [9].…”

Section: Introductionmentioning

confidence: 99%

The relationship between Chlamydia pneumoniae infection and TNF-α in cardiovascular disease patients

Nasser

Ismael

Halbosiy

2018

ijs

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Over the last few years the role of microorganisms in the pathogenesis of atherosclerosis has been widely discussed. Advance in basic science have established a fundamental role for inflammation immediating all stages of cardiovascular diseases. Chlamydia pneumoniae activates immune cells to produce cytokines such us TNF-α that are important contributor to atherosclerosis. All blood samples were assayed for molecular detection of Chlamydia pneumoniae by using conventional polymerase chain reaction (PCR) relying on16SrRNAand the level of serum TNF-α measured by enzyme linked immunosorbent assay (ELISA).Seventy patients who suffering from CVD (angina, myocardial Infarction and atherosclerosis) aged between 33-86 years have been investigated and compared to twenty of apparently healthy individuals were studies as control group. Twenty six sample (37.14) %detected positive results for Chlamydia pneumoniae by PCR techniques in patient group, while all control group were negative, furthermore current study revealed a highly significant elevation (p<0.01) in the mean level of TNF-α in sera of patients with CVD compared to control group. Also there were considerable differences in the level of TNF-α between Chlamydia pneumoniae positive and negative within the patient group. The present study concludes there is a significant proportion among patients who infected with C. Pneumoniae and these bacteria play an essential role in the pathogenesis of CVD through stimulation of the inflammatory response.

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Pro and Anti‐Inflammatory Cytokine Networks in Atherosclerosis

Cited by 6 publications

References 52 publications

Evaluation of the Effect of Andrographolide on Atherosclerotic Rabbits Induced byPorphyromonas gingivalis

Evaluation of the Effect of Andrographolide on Atherosclerotic Rabbits Induced byPorphyromonas gingivalis

Integrin signaling in atherosclerosis

The relationship between Chlamydia pneumoniae infection and TNF-α in cardiovascular disease patients

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