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 ◽  
...  
2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Sandra Armengol Lopez ◽  
Kathleen M. Botham ◽  
Charlotte Lawson

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.


2007 ◽  
Vol 35 (3) ◽  
pp. 464-465 ◽  
Author(s):  
C. Bentley ◽  
F. Bejta ◽  
C. De Pascale ◽  
M. Avella ◽  
C.P.D. Wheeler-Jones ◽  
...  

In early atherosclerosis the frequency of activated monocytes in the peripheral circulation is amplified, and migration of monocytes into the walls of the aorta and large arteries is increased, due partly to de novo expression or activation of monocyte adhesion molecules. Although there is increasing evidence that CMRs (chylomicron remnants) are strongly atherogenic, the outcomes of interactions between blood monocytes and circulating CMRs are not known. Here, we have studied the effects of CRLPs (CMR-like particles) on THP-1 human monocyte oxidative burst. The particles induced a significant increase in reactive oxygen species within 1 h, which persisted for 24 h. We suggest that monocyte–CMR interactions may be important in early atherosclerosis when many activated monocytes are found in susceptible areas of the artery wall.


2001 ◽  
Vol 386 (2) ◽  
pp. 221-226 ◽  
Author(s):  
Fabian Moraga ◽  
Stefan Lindgren ◽  
Sabina Janciauskiene

2008 ◽  
Vol 9 (2) ◽  
pp. 99-100
Author(s):  
C. Bentley ◽  
N. Hathaway ◽  
C. DePascale ◽  
M. Avella ◽  
C. Wheeler-Jones ◽  
...  

2004 ◽  
Vol 321 (3) ◽  
pp. 592-600 ◽  
Author(s):  
Sabina Janciauskiene ◽  
Susanne Larsson ◽  
Peter Larsson ◽  
Robert Virtala ◽  
Lennart Jansson ◽  
...  

2009 ◽  
Vol 24 (4) ◽  
pp. 805-811 ◽  
Author(s):  
Sean B. Orenstein ◽  
Yi Qiao ◽  
Manjot Kaur ◽  
Ulrike Klueh ◽  
Don L. Kreutzer ◽  
...  

2021 ◽  
Vol 91 ◽  
pp. 107270
Author(s):  
Caroline B.K. Mathiesen ◽  
Asha M. Rudjord-Levann ◽  
Monika Gad ◽  
Jesper Larsen ◽  
Finn Sellebjerg ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Om Makwana ◽  
Gina A. Smith ◽  
Hannah E. Flockton ◽  
Gary P. Watters ◽  
Frazer Lowe ◽  
...  

AbstractAtherosclerosis is a complex process involving progressive pathological events, including monocyte adhesion to the luminal endothelial surface. We have developed a functional in vitro adhesion assay using BioFlux microfluidic technology to investigate THP-1 (human acute monocytic leukaemia cell) monocyte adhesion to human aortic endothelial cells (HAECs). The effect of whole smoke conditioned media (WSCM) generated from University of Kentucky reference cigarette 3R4F, electronic cigarette vapour conditioned media (eVCM) from an electronic nicotine delivery system (ENDS) product (Vype ePen) and nicotine on monocyte adhesion to HAECs was evaluated. Endothelial monolayers were grown in microfluidic channels and exposed to 0–1500 ng/mL nicotine or nicotine equivalence of WSCM or eVCM for 24 h. Activated THP-1 cells were perfused through the channels and a perfusion, adhesion period and wash cycle performed four times with increasing adhesion period lengths (10, 20, 30 and 40 min). THP-1 cell adhesion was quantified by counting adherent cells. WSCM induced dose-dependent increases in monocyte adhesion compared to vehicle control. No such increases were observed for eVCM or nicotine. Adhesion regulation was linked to increased ICAM-1 protein expression. Staining of ICAM-1 in HAECs and CD11b (MAC-1) in THP-1 cells demonstrated adhesion molecule co-localisation in BioFlux plates. The ICAM-1 adhesion response to WSCM was downregulated by transfecting HAECs with ICAM-1 siRNA. We conclude that the BioFlux system is able to model human monocyte adhesion to primary human endothelial cells in vitro and WSCM drives the greatest increase in monocyte adhesion via a mechanism involving endothelial ICAM-1 expression.


1997 ◽  
Vol 43 (1) ◽  
pp. 6-10 ◽  
Author(s):  
Barbara Magri ◽  
Paola Viganò ◽  
Gabriele Rossi ◽  
Edgardo Somigliana ◽  
Barbara Gaffuri ◽  
...  

Author(s):  
Sarah McCarrick ◽  
Valentin Romanovski ◽  
Zheng Wei ◽  
Elin M. Westin ◽  
Kjell-Arne Persson ◽  
...  

AbstractWelders are daily exposed to various levels of welding fumes containing several metals. This exposure can lead to an increased risk for different health effects which serves as a driving force to develop new methods that generate less toxic fumes. The aim of this study was to explore the role of released metals for welding particle-induced toxicity and to test the hypothesis that a reduction of Cr(VI) in welding fumes results in less toxicity by comparing the welding fume particles of optimized Cr(VI)-reduced flux-cored wires (FCWs) to standard FCWs. The welding particles were thoroughly characterized, and toxicity (cell viability, DNA damage and inflammation) was assessed following exposure to welding particles as well as their released metal fraction using cultured human bronchial epithelial cells (HBEC-3kt, 5–100 µg/mL) and human monocyte-derived macrophages (THP-1, 10–50 µg/mL). The results showed that all Cr was released as Cr(VI) for welding particles generated using standard FCWs whereas only minor levels (< 3% of total Cr) were released from the newly developed FCWs. Furthermore, the new FCWs were considerably less cytotoxic and did not cause any DNA damage in the doses tested. For the standard FCWs, the Cr(VI) released in cell media seemed to explain a large part of the cytotoxicity and DNA damage. In contrast, all particles caused rather similar inflammatory effects suggesting different underlying mechanisms. Taken together, this study suggests a potential benefit of substituting standard FCWs with Cr(VI)-reduced wires to achieve less toxic welding fumes and thus reduced risks for welders.


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