VLDL Modulates the Cytokine Secretion Profile to a Proinflammatory Pattern

Sampedro, María Cecilia; Motrán, Cristina; Gruppi, Adriana; Kivatinitz, Silvia C.

doi:10.1006/bbrc.2001.5202

Cited by 9 publications

(4 citation statements)

References 25 publications

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“…It is well established that elevated levels of plasma VLDL are considered to be an independent risk factor for the progression of atherosclerosis (41,42). VLDL has also been shown to potentiate the inflammatory processes associated with atherosclerosis by 1) enhancing the expression of tumor necrosis factor α and interleukin-1β expression in macrophages (29,30), and 2) modulating the cytokine secretion profile of lymphocytes to a predominantly proinflammatory response (28). Previous studies have also demonstrated that cholic acid can activate genes associated with hepatic fibrosis, while the cholesterol component of the atherogenic diet was found to induce genes responsible for the acute inflammatory response (31).…”

Section: Discussionmentioning

confidence: 99%

Hyperhomocysteinemia induced by methionine supplementation does not independently cause atherosclerosis in C57BL/6J mice

Zhou¹,

Werstuck²,

Lhoták³

et al. 2008

FASEB j.

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A causal relationship between diet-induced hyperhomocysteinemia (HHcy) and accelerated atherosclerosis has been established in apolipoprotein E-deficient (apoE −/− ) mice. However, it is not known whether the proatherogenic effect of HHcy in apoE −/− mice is independent of hyperlipidemia and/or deficiency of apoE. In this study, a comprehensive dietary approach using C57BL/6J mice was used to investigate whether HHcy is an independent risk factor for accelerated atherosclerosis or dependent on additional dietary factors that increase plasma lipids and/or inflammation. C57BL/ 6J mice at 4 wk of age were divided into 6 dietary groups: chow diet (C), chow diet + methionine (C+M), western-type diet (W), western-type diet + methionine (W+M), atherogenic diet (A), or atherogenic diet + methionine (A+M). After 2, 10, 20, or 40 wk on the diets, mice were sacrificed, and the levels of total plasma homocysteine, cysteine, and glutathione, as well as total plasma cholesterol and triglycerides were analyzed. Aortic root sections were examined for atherosclerotic lesions. HHcy was induced in all groups supplemented with methionine, compared to diet-matched control groups. Plasma total cholesterol was significantly increased in mice fed the W or A diet. However, the W diet increased LDL/IDL and HDL levels, while the A diet significantly elevated plasma VLDL and LDL/IDL levels without increasing HDL. No differences in plasma total cholesterol levels or lipid profiles were observed between methionine-supplemented groups and the diet-matched control groups. Early atherosclerotic lesions containing macrophage foam cells were only observed in mice fed the A or A + M diet. Furthermore, lesion size was significantly larger in the A + M group compared to the A group at 10 and 20 wk; however, mature lesions were never observed even after 40 wk on these diets. The presence of lymphocytes, increased hyaluronan staining, and the expression of endoplasmic reticulum (ER) stress markers were also increased in atherosclerotic lesions from the A + M group. Taken together, these results suggest that HHcy does not independently cause atherosclerosis in C57BL/6J mice even in the presence of increased total Clinical and epidemiological studies have established that elevated plasma total homocysteine (tHcy) is an independent risk factor for cardiovascular disease and stroke (1,2). Furthermore, accelerated atherosclerosis has been demonstrated in apolipoprotein E-deficient (apoE −/− ) mice with dietary hyperhomocysteinemia (HHcy) (3-5) and in cystathionine β-synthase (CBS)/apoE −/− double-knockout mice (6). These findings suggest that HHcy accelerates atherogenesis in a hyperlipidemic mouse model that develops spontaneous atherosclerosis. However, a causal relationship between atherogenesis and HHcy has not been established in other species, including rats, rabbits, pigs, and primates (7-10).Patients with inborn errors of methionine metabolism due to deficiencies in CBS or 5,10-methylenetetrahydrofolate reductase (MTHFR) present with severe...

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Section: Discussionmentioning

confidence: 99%

Hyperhomocysteinemia induced by methionine supplementation does not independently cause atherosclerosis in C57BL/6J mice

Zhou¹,

Werstuck²,

Lhoták³

et al. 2008

FASEB j.

View full text Add to dashboard Cite

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“…There are numerous interactions between inflammatory cytokines and lipoprotein metabolism. For instance, the inflammatory response of endothelial cells and macrophages has been shown to be induced by the presence of TRLs (35, 36). Furthermore, the proinflammatory condition that prevails during the postprandial period has been recently associated with a TG‐specific activation of monocytes and neutrophils (37).…”

Section: Discussionmentioning

confidence: 99%

Postprandial Variations of Plasma Inflammatory Markers in Abdominally Obese Men

Blackburn

Després

Lamarche

et al. 2006

Obesity

123

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variations of plasma inflammatory markers in abdominally obese men. Obesity. 2006;14:1747-1754. Objective: Abdominal obesity is associated with a fasting proinflammatory condition. However, not much is known of the potential variations in circulating inflammatory markers after food intake. The purpose of the present study was to examine postprandial changes in plasma tumor necrosis factor (TNF)-␣, interleukin (IL)-6, and C-reactive protein (CRP) concentrations in men and their potential associations with fat distribution and metabolic profile variables. Research Methods and Procedures: Thirty-eight men were given a high-fat meal in the morning after an overnight fast, and TNF-␣, IL-6, and CRP levels were measured in plasma at 0, 4, and 8 hours after the meal. Physical and metabolic profiles were also assessed for each participant. Results: We observed a substantial increase in circulating IL-6 levels (p Ͻ 0.0001) after the meal. Although postprandial variations in circulating TNF-␣ levels across time failed to reach statistical significance (p ϭ 0.02), we noted a significant decrease in plasma TNF-␣ concentrations 4 hours (Ϫ10%, p Ͻ 0.001 vs. 0 hours) after food intake. Plasma CRP levels were not affected by the fat load. We also noted that insulin-sensitive individuals displayed a less pronounced inflammatory response after food intake than insulin-resistant subjects. Discussion: Results of the present study show that consumption of a high-fat meal leads to an increase in plasma IL-6 concentrations and transient decrease in circulating TNF-␣ levels in overweight men. Our results suggest a possible role of insulin resistance in the modulation of the postprandial inflammatory response, which could, in turn, contribute to worsen the state of insulin resistance.

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“…Cultures were carried out for 96-h period since the mitogenic effect of Con A is fully displayed at this time, after longer culture times most cells die and the percentage of viable cells is very low to perform this kind of experiments [14]. Cultures containing 1 Â 10 6 PBMC were cultured in the presence of phytohaemagglutinin (PHA) (5 mg/ml) with or without mannan (0.6 mg/ml) in a total volume of 2 ml for 96 h [15]. The tumoral cell lines were cultured without mitogen with or without mannan (0.6 mg/ml).…”

Section: Cell Proliferation Assaysmentioning

confidence: 99%