A more mature phenotype of blood mononuclear phagocytes is induced by fluvastatin treatment in hypercholesterolemic patients with coronary heart disease

Rothe, Gregor; Herr, Alexandra S.; Stöhr, Josef; Abletshauser, C.; Weidinger, Gottfried; Schmitz, Gerd

doi:10.1016/s0021-9150(99)00061-1

Cited by 72 publications

(59 citation statements)

References 55 publications

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“…Data in the literature on the effect of these substances on monocytic receptor expression are scarce. Statin treatment was most common in the diabetes group and these substances have been shown to decrease the expression of CD14 on monocytes [10]. In the event that this influenced the results in this study, it could have been by reducing the differences.…”

Section: Discussionmentioning

confidence: 71%

Monocytic expression of CD14 and CD18, circulating adhesion molecules and inflammatory markers in women with diabetes mellitus and impaired glucose tolerance

et al. 2004

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Aims/hypothesis. Type 2 diabetes is a major risk factor for cardiovascular disease. Monocyte recruitment and inflammatory activation are crucial steps in the development of atherosclerosis and several receptors are involved in these processes. The aim of this study was to investigate levels of CD14 and the β 2 -integrin subunits CD11b and CD18 on monocytes from women with diabetes or impaired glucose tolerance. Methods. A population-based sample of 112 Swedish women, who were aged 64 years and had diabetes mellitus or impaired or normal glucose tolerance, was investigated. Cell surface receptors were analysed with flow cytometry and serum inflammation markers and soluble adhesion molecules with enzyme-linked methods.Results. The monocytic CD14 expression and serum levels of C-reactive protein, IL-6 and soluble adhesion molecules were higher in the diabetes group than in the group with normal glucose tolerance. Monocytic CD18 was elevated both in the diabetes and in the impaired glucose tolerance groups. The levels of monocytic surface markers correlated with BMI and to a lesser extent with glycaemic control. Conclusions/interpretation. The increased monocytic expression of important surface receptors together with elevated serum inflammation markers supports the concept of increased inflammation in type 2 diabetes and may be an important factor for the risk of atherosclerosis.

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Section: Discussionmentioning

confidence: 71%

Monocytic expression of CD14 and CD18, circulating adhesion molecules and inflammatory markers in women with diabetes mellitus and impaired glucose tolerance

et al. 2004

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“…38 Fc␥RI (CD64) binds monomeric as well as aggregated human IgG with high affinity, whereas Fc␥RII (CD32) and Fc␥RIII (CD16) are receptors of lower affinity that only bind IgG in the form of ICs with a preference for IgG 1 and IgG 3 . 39,40 Immunohistochemical analysis has shown the presence of all three classes of Fc␥Rs in human atherosclerotic coronary arteries, where the majority of the receptor-bearing cells were of mononuclear phagocyte origin.…”

Section: Discussionmentioning

confidence: 99%

OxLDL–IgG Immune Complexes Induce Survival of Human Monocytes

Oksjoki

Kovanen

Lindstedt

et al. 2006

ATVB

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Objective-Immune complexes containing oxidatively modified low-density lipoprotein (oxLDL) particles are deposited in human atherosclerotic lesions during atherogenesis. Here we studied whether OxLDL-IgG immune complexes (OxLDL-IgG ICs) affect survival of human monocytes. Methods and Results-As demonstrated by light microscopy, and analysis of cell proliferation, caspase-3 activity, and DNA fragmentation, OxLDL-IgG ICs promoted survival of cultured human monocytes by decreasing their spontaneous apoptosis. OxLDL-IgG ICs induced a concentration-dependent production of the major monocyte growth factor, monocyte colony-stimulating factor (M-CSF), by the monocytes, but its inhibition was without effect on OxLDL-IgG IC-induced monocyte survival. Rather, OxLDL-IgG ICs induced rapid phosphorylation of Akt, suggesting a direct anti-apoptotic effect mediated by cross-linking of Fc␥ receptors. Experiments with receptor blocking antibodies revealed that the OxLDL-IgG IC-induced monocyte survival was mediated by Fc␥ receptor I. Key Words: atherosclerosis Ⅲ monocytes Ⅲ oxLDL A therosclerosis is characterized by early accumulation of lipids and macrophages in the intimal layer of the arterial wall. Lipids, mainly derived from serum low-density lipoprotein (LDL) particles, accumulate in the extracellular matrix of the intima, were they are exposed to various modifications, such as oxidation. 1 The process may begin early in life as epitopes of oxLDL are found the aortic intima of human fetuses of hypercholesterolemic women, and this is followed by infiltration of monocytes in the intima. 2 OxLDL is recognized and taken up by macrophages via scavenger receptors, which are then transformed into lipid-filled foam cells. Modified lipids on the surface of oxLDL are biologically active and are recognized by various pattern recognition receptors of the innate immune system, notably by the Toll-like receptor 4 (TLR4). 3,4 OxLDL is also able to activate the adaptive immune system when antigen-presenting cells present peptides derived from oxLDL particle on MHC class II molecules for recognition by CD4 ϩ T cells, 5 which then leads to the production of antibodies specific for oxLDL. Consistently, human atherosclerotic lesions contain clones of CD4 ϩ T cells that recognize epitopes of oxLDL and respond to oxLDL stimulation by proliferation and cytokine production. 6 Moreover, antibodies against oxLDL are present in the circulation, and their levels have been shown to correlate positively with cardiovascular disease and its complications. [7][8][9] Human atherosclerotic lesions also contain IgG that recognizes oxLDL and OxLDL-IgG immune complexes (OxLDL-IgG IC). 10 When added to cultured macrophages, OxLDL-IgG ICs promote foam cell formation and induce the production of proinflammatory cytokines, oxygen radicals, and matrix metalloproteinases by the macrophages. [11][12][13] Infiltration of monocytes into the arterial intima involves their attachment to activated endothelium via vascular cell adhesion molecule (VCAM)-1, and transmigrat...

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“…LPS is probably one factor responsible for the lipid profile changes, but sCD14 and, especially, the distribution of CD14-positive monocytes may also be involved in the regulation of serum lipid levels [36,37]. In vitro experiments have shown that the availability of sCD14 may determine the efficacy of lipid transfer from cells to extracellular space [38].…”

Section: Discussionmentioning

confidence: 99%

Effect of CD14 promoter polymorphism andH. pyloriinfection and its clinical outcomes on circulating CD14

Karhukorpi¹,

Yan²,

Niemelä

et al. 2002

Clinical and Experimental Immunology

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SUMMARYCD14 is a pattern recognition receptor on the membranes of monocytes and macrophages for several microbial products, of which lipopolysaccharide (LPS) is the best known. A shed form of CD14 is present in serum. As the CD14 gene promoter polymorphism -159C/T and some bacterial infections may affect the sCD14 levels, we compared the impact of both the CD14 promoter polymorphism and Helicobacter pylori infection on serum sCD14 levels in 201 dyspeptic patients (group 1) who had undergone gastroscopy, and 127 staff members (group 2) with no endoscopy. sCD14 was measured from the sera by a commercial enzyme immunoassay (EIA), and CD14 genotyping was carried out with PCR. Helicobacter pylori infection was detected by serology and/or culture or PCR. sCD14 levels were elevated in the subjects carrying the T allele (CT or TT genotype) in both groups when compared with subjects with the CC genotype. Overall, H. pylori-positive subjects tended to have higher sCD14 levels compared with H. pylori-negative subjects. In group 1 consisting of dyspeptic patients, those with gastric ulcer, gastric erosion or duodenal ulcer had significantly elevated levels of sCD14 compared with the patients with normal endoscopic findings or macroscopic gastritis. The recent use of NSAIDs was also associated with enhanced sCD14. Thus, we were able to show several factors, one genetic and the other environmental (H. pylori infection and mucosal lesion), to have an impact on sCD14.

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A more mature phenotype of blood mononuclear phagocytes is induced by fluvastatin treatment in hypercholesterolemic patients with coronary heart disease

Cited by 72 publications

References 55 publications

Monocytic expression of CD14 and CD18, circulating adhesion molecules and inflammatory markers in women with diabetes mellitus and impaired glucose tolerance

Monocytic expression of CD14 and CD18, circulating adhesion molecules and inflammatory markers in women with diabetes mellitus and impaired glucose tolerance

OxLDL–IgG Immune Complexes Induce Survival of Human Monocytes

Effect of CD14 promoter polymorphism andH. pyloriinfection and its clinical outcomes on circulating CD14

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