scholarly journals The Oxidative State of Chylomicron Remnants Influences Their Modulation of Human Monocyte Activation

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Sandra Armengol Lopez ◽  
Kathleen M. Botham ◽  
Charlotte Lawson
Keyword(s):  
Human Monocyte ◽  
Ros Production ◽  
Human Monocytes ◽  
Monocyte Activation ◽  
Monocyte Chemoattractant Protein 1 ◽  
Monocyte Chemoattractant ◽  
Chylomicron Remnants ◽  
Oxidative State ◽  
Stimulation Of

Chylomicron remnants (CMRs) contribute directly to human monocyte activationin vitro, by increasing reactive oxygen species (ROS) production and cell migration. In this study, the effects of the oxidative state of CMR on the degree of monocyte activation was investigated. CMR-like particles (CRLPs) were prepared in three different oxidative states, normal (CRLPs), protected from oxidation by incorporation of the antioxidant, probucol (pCRLPs), or oxidised with CuSO4(oxCRLPs). Lipid accumulation and ROS production were significantly increased in primary human monocytes incubated with CRLPs, whilst secretion on monocyte chemoattractant protein-1 was reduced, but oxCRLPs had no additional effect. In contrast, pCRLPs were taken up by monocytes to a lesser extent and had no significant effect on ROS or MCP-1 secretion. These studies suggest that the oxidative state of CMRs modulates their stimulation of the activation of peripheral blood human monocytes and that dietary antioxidants may provide some protection against these atherogenic effects.

Induction of Monocyte Chemoattractant Protein-1 Synthesis in Human Monocytes During Transendothelial Migration In Vitro

1995 ◽  
Vol 76 (5) ◽  
pp. 750-757 ◽  
Author(s):  
Masafumi Takahashi ◽  
Jun-Ichi Masuyama ◽  
Uichi Ikeda ◽  
Tadashi Kasahara ◽  
Sei-Ichi Kitagawa ◽  
...  
Keyword(s):  
Transendothelial Migration ◽  
Human Monocytes ◽  
Monocyte Chemoattractant Protein 1 ◽  
Monocyte Chemoattractant ◽  
Monocyte Chemoattractant Protein

Effects of Zotarolimus (ABT-578), Sirolimus, Paclitaxel and Dexamethasone on Cytokine Production by Human Monocytes In Vitro.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 3866-3866
Author(s):  
Lanlan Li ◽  
Sandra E. Burke ◽  
Matthew M. Mack
Keyword(s):  
Cytokine Production ◽  
Coronary Intervention ◽  
Human Monocytes ◽  
Cytokine Release ◽  
Monocyte Chemoattractant Protein 1 ◽  
Monocyte Chemoattractant ◽  
Percutaneous Coronary ◽  
Drug Eluting ◽  
Necrosis Factor

Abstract Introduction: Percutaneous coronary intervention (PCI) and stenting are common therapies used to mitigate symptomatic coronary artery stenosis. These mechanical procedures are invariably associated with local and systemic inflammation, including activation and cytokine release from monocytes/macrophages, which are major stimuli for smooth muscle cell proliferation, migration and restenosis. Drug-eluting stents (DES) may potentially attenuate this inflammatory response, provided that the drug has antiinflammatory potency. This study was conducted to determine the effects of common DES agents on the generation of proinflammatory cytokines by stimulated human monocytes in vitro. Methods: The production of monocyte chemoattractant protein-1 (MCP-1), tumor necrosis factor-a (TNF-a) and interleukin-6 (IL-6) by LPS-stimulated monocytes was determined by ELISA after exposure to either zotarolimus (ABT-578), sirolimus, dexamethasone or paclitaxel. Results: The results showed that zotarolimus (ABT-578) and sirolimus were potent inhibitors of MCP-1 production (IC50 = 2.6 ± 0.2 and 5.9 ± 1.9 nM, respectively). Dexamethasone also inhibited MCP-1 production, but it was less potent (IC50 = 626.9 ± 60.8 nM). TNF-a and IL-6 production were dose-dependently inhibited by dexamethasone (IC50 = 5.5 ± 0.2 and 13.0 ± 3.7 nM, respectively). However, the production of neither cytokine was significantly inhibited by exposure to zotarolimus or sirolimus. Stimulated monocytes were not affected by paclitaxel; cytokine release after exposure to paclitaxel was no different from controls. Conclusions: Zotarolimus and sirolimus are potent inhibitors of MCP-1 secretion by stimulated monocytes in culture. Dexamethasone is a less potent inhibitor of MCP-1 secretion, but effectively inhibits the release of TNF-a and IL-6. The anti-restenotic effect of these agents may, in part, be due to their potent antiinflammatory properties.

Zika Virus Infects Newborn Monocytes Without Triggering a Substantial Cytokine Response

2019 ◽  
Vol 220 (1) ◽  
pp. 32-40 ◽  
Author(s):  
Fabio Seiti Yamada Yoshikawa ◽  
Anna Julia Pietrobon ◽  
Anna Cláudia Calvielli Castelo Branco ◽  
Nátalli Zanete Pereira ◽  
Luanda Mara da Silva Oliveira ◽  
...  
Keyword(s):  
Viral Entry ◽  
Zika Virus ◽  
Human Monocyte ◽  
Interleukin 10 ◽  
Cytokine Response ◽  
Monocyte Chemoattractant Protein 1 ◽  
Monocyte Chemoattractant ◽  
Favorable Environment ◽  
Adult Cells

Abstract Zika virus (ZIKV) is a clinically important flavivirus that can cause neurological disturbances in newborns. Here, we investigated comparatively the outcome of in vitro infection of newborn monocytes by ZIKV. We observed that neonatal cells show defective production of interleukin 1β, interleukin 10, and monocyte chemoattractant protein 1 in response to ZIKV, although they were as efficient as adult cells in supporting viral infection. Although CLEC5A is a classical flavivirus immune receptor, it is not essential to the cytokine response, but it regulates the viral load only in adult cells. Greater expression of viral entry receptors may create a favorable environment for viral invasion in neonatal monocytes. We are the first to suggest a role for CLEC5A in human monocyte infectivity and to show that newborn monocytes are interesting targets in ZIKV pathogenesis, owing to their ability to carry the virus with only a partial triggering of the immune response, creating a potentially favorable environment for virus-related pathologies in young individuals.

scholarly journals An Antagonist of Monocyte Chemoattractant Protein 1 (MCP-1) Inhibits Arthritis in the MRL-lpr Mouse Model

1997 ◽  
Vol 186 (1) ◽  
pp. 131-137 ◽  
Author(s):  
Jiang-Hong Gong ◽  
Leslie G. Ratkay ◽  
J. Douglas Waterfield ◽  
Ian Clark-Lewis
Keyword(s):  
Mouse Model ◽  
Competitive Inhibition ◽  
Human Monocyte ◽  
Daily Injection ◽  
Human Rheumatoid Arthritis ◽  
Monocyte Chemoattractant Protein 1 ◽  
Monocyte Chemoattractant ◽  
Monocyte Chemoattractant Protein

An antagonist of human monocyte chemoattractant protein (MCP)-1, which consists of MCP-1(9-76), had previously been characterized and shown to inhibit MCP-1 activity in vitro. To test the hypothesis that, by inhibiting endogenous MCP-1, the antagonist has antiinflammatory activity in vivo, we examined its effect in the MRL-lpr mouse model of arthritis. This strain spontaneously develops a chronic inflammatory arthritis that is similar to human rheumatoid arthritis. Daily injection of the antagonist, MCP-1(9-76), prevented the onset of arthritis as monitored by measuring joint swelling and by histopathological evaluation of the joints. In contrast, controls treated with native MCP-1 had enhanced arthritis symptoms, indicating that the inhibitory effect is specific to the antagonist. In experiments where the antagonist was given only after the disease had already developed, there was a marked reduction in symptoms and histopathology, although individuals varied in the magnitude of the response. The mechanism of inhibition of disease is not known, although the results suggest that it could be more complex than the competitive inhibition of ligand binding that is observed in vitro. The demonstration of the beneficial effects of an MCP-1 antagonist in arthritis suggests that chemokine receptor antagonists could have therapeutic application in inflammatory diseases.

scholarly journals Influence of chylomicron remnants on human monocyte activation in vitro

2011 ◽  
Vol 21 (11) ◽  
pp. 871-878 ◽  
Author(s):  
C. Bentley ◽  
N. Hathaway ◽  
J. Widdows ◽  
F. Bejta ◽  
C. De Pascale ◽  
...  
Keyword(s):  
Human Monocyte ◽  
Monocyte Activation ◽  
Chylomicron Remnants

scholarly journals Hyaluronan induces monocyte chemoattractant protein-1 expression in renal tubular epithelial cells.

1998 ◽  
Vol 9 (12) ◽  
pp. 2283-2290
Author(s):  
B Beck-Schimmer ◽  
B Oertli ◽  
T Pasch ◽  
R P Wüthrich
Keyword(s):  
Protein Expression ◽  
Renal Injury ◽  
De Novo ◽  
Kidney Diseases ◽  
Monocyte Chemoattractant Protein 1 ◽  
Monocyte Chemoattractant ◽  
Monocyte Chemoattractant Protein ◽  
Mrna And Protein Expression ◽  
Renal Tubular

Hyaluronan (HA) is a nonsulfated glycosaminoglycan that accumulates in the renal interstitium in immune-mediated kidney diseases. The functional significance of such HA deposition in the kidney has not been elucidated. Several studies have suggested that HA may exhibit proinflammatory effects. Since chemokines such as monocyte chemoattractant protein-1 (MCP-1) play an important role in the recruitment of leukocytes in renal injury, this study tested whether HA and its fragments could promote MCP-1 production by renal parenchymal cells. Mouse cortical tubular cells were stimulated with fragmented HA or with high molecular weight HA (Healon) in vitro and were examined for MCP-1 expression. Fragmented HA, but not Healon, increased MCP-1 mRNA within 30 min with a peak after 2 h. In addition, a 10-fold increase of MCP-1 protein in the supernatant was found after a 6-h stimulation with fragmented HA. The enhanced MCP-1 mRNA and protein expression in response to HA was dose-dependent between 1 and 100 microg/ml. Upregulation of MCP-1 protein production could be blocked by preincubation with actinomycin D or cycloheximide, suggesting that MCP-1 mRNA and protein expression in response to HA are based on de novo synthesis. The HA-stimulated MCP-1 production was also inhibited with anti-CD44 antibodies, suggesting that MCP-1 is upregulated at least in part by signaling through CD44. In summary, fragmented HA markedly stimulates renal tubular MCP-1 production by mechanisms that involve binding to the HA receptor CD44. It is hypothesized that the accumulation of HA in immune renal injury could participate in the recruitment and activation of inflammatory cells in vivo through production of MCP-1.

scholarly journals Antibacterial Effects of Levofloxacin, Erythromycin, and Rifampin in a Human Monocyte System againstLegionella pneumophila

1998 ◽  
Vol 42 (12) ◽  
pp. 3153-3156 ◽  
Author(s):  
Aldona L. Baltch ◽  
Raymond P. Smith ◽  
Mary A. Franke ◽  
Phyllis B. Michelsen
Keyword(s):  
Antibacterial Activity ◽  
Legionella Pneumophila ◽  
Human Monocyte ◽  
Antibacterial Activities ◽  
Human Monocytes ◽  
Antibacterial Effects ◽  
In Vitro System ◽  
Time Period ◽  
Time Periods

ABSTRACT The antibacterial activities of levofloxacin, erythromycin, and rifampin against intracellular Legionella pneumophilaL-1033, serogroup 1, were studied. In an in vitro system utilizing adherent human monocytes, L. pneumophila L-1033, a phagocytosis time period of 1 h, and antibiotic (levofloxacin, erythromycin, and/or rifampin) at 1 to 10 times the MIC, the CFU/ml values for the monocyte lysate were determined during 0- to 4-day time periods. The decrease in CFU/ml with levofloxacin at pH 7.4 was rapid, occurring within 24 h, and was drug concentration dependent (P < 0.01). The decrease in CFU with rifampin was first observed at 48 h (P < 0.01), while only a minimal decrease in CFU/ml was observed with erythromycin. Combination of levofloxacin and rifampin and of levofloxacin and erythromycin at ten times their MICs significantly decreased the CFU/ml value (P < 0.01), to the value attained by levofloxacin alone, while combination of rifampin and erythromycin did not. Removal of levofloxacin after 24 h of incubation resulted in regrowth ofL. pneumophila L-1033, while a continued slow decrease in CFU/ml was seen following rifampin removal; CFU/ml values were unaffected by the removal of erythromycin. At 4 days, and even in assays performed following antibiotic removal, the CFU/ml value continued to be lower in the levofloxacin and rifampin assays than in the assays with erythromycin. Levofloxacin had a significantly higher bactericidal activity against L. pneumophila L-1033 than erythromycin or rifampin. In these assays, the addition of erythromycin or rifampin did not affect the antibacterial activity of levofloxacin.

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