scholarly journals Monocyte Activation from Interferon-α in HIV Infection Increases Acetylated LDL Uptake and ROS Production

2014 ◽  
Vol 34 (10) ◽  
pp. 822-828 ◽  
Author(s):  
Lynn Pulliam ◽  
Cyrus Calosing ◽  
Bing Sun ◽  
Carl Grunfeld ◽  
Hans Rempel
Cytokine ◽  
2001 ◽  
Vol 14 (1) ◽  
pp. 56-62 ◽  
Author(s):  
Eva Stylianou ◽  
Pål Aukrust ◽  
Fredrik Müller ◽  
Ingvild Nordøy ◽  
Stig S. Frøland

2017 ◽  
Vol 14 (12) ◽  
pp. 960-962 ◽  
Author(s):  
Hua Liang ◽  
Zhe Xie ◽  
Tao Shen

PLoS ONE ◽  
2020 ◽  
Vol 15 (1) ◽  
pp. e0218905 ◽  
Author(s):  
Julia Ickler ◽  
Sandra Francois ◽  
Marek Widera ◽  
Mario L. Santiago ◽  
Ulf Dittmer ◽  
...  

EBioMedicine ◽  
2020 ◽  
Vol 62 ◽  
pp. 103129
Author(s):  
Sophie Novelli ◽  
Camille Lécuroux ◽  
Cécile Goujard ◽  
Jacques Reynes ◽  
Agnès Villemant ◽  
...  

2014 ◽  
Vol 210 (9) ◽  
pp. 1396-1406 ◽  
Author(s):  
Eleanor M. P. Wilson ◽  
Amrit Singh ◽  
Katherine Huppler Hullsiek ◽  
Dave Gibson ◽  
W. Keith Henry ◽  
...  

Blood ◽  
2011 ◽  
Vol 117 (7) ◽  
pp. 2189-2199 ◽  
Author(s):  
David Favre ◽  
Cheryl A. Stoddart ◽  
Brinda Emu ◽  
Rebecca Hoh ◽  
Jeffrey N. Martin ◽  
...  

Abstract HIV infection can result in depletion of total CD4+ T cells and naive CD8+ T cells, and in the generation of dysfunctional effector CD8+ T cells. In this study, we show that naive CD8+ T cells in subjects with progressive HIV disease express low levels of CD8α and CD8β chains. Such naive CD8low T cells display broad signaling defects across the T-cell receptor complex, and their appearance correlates with generalized up-regulation of major histocompatibility complex class I (MHC-I) antigens on peripheral blood mononuclear cells (PBMCs). To explore a causal link between increased MHC-I up-regulation and the generation of naive CD8low T cells, we used the humanized SCID-hu Thy/Liv mouse model to show that HIV infection of the thymus and interferon α (IFNα) treatment alone result in MHC-I up-regulation and in the generation of dysfunctional CD3highCD8+CD4− single-positive 8 (SP8) thymocytes with low expression of CD8. We suggest that dysfunctional naive CD8low T cells are generated as a result of IFNα-mediated up-regulation of MHC-I on stromal cells in the thymus and antigen-presenting cells in the periphery, and that dysfunction in this naive compartment contributes to the immunodeficiency of HIV disease. This study is registered at www.clinicaltrials.gov as NCT00187512.


2017 ◽  
Vol 4 (1) ◽  
Author(s):  
Meagan P. O’Brien ◽  
Peter W. Hunt ◽  
Douglas W. Kitch ◽  
Karin Klingman ◽  
James H. Stein ◽  
...  

Abstract Background Immune activation persists despite suppressive antiretroviral therapy (ART) in human immunodeficiency virus (HIV) infection and predicts non-Acquired Immune Deficiency Syndrome (AIDS) comorbidities including cardiovascular disease. Activated platelets play a key role in atherothrombosis and inflammation, and platelets are hyperactivated in chronic HIV infection. Aspirin is a potent inhibitor of platelet activation through the cyclooxygenase-1 (COX-1) pathway. We hypothesized that platelet activation contributes to immune activation and that aspirin would reduce immune activation and improve endothelial function in ART-suppressed HIV-infected individuals. Methods In this prospective, double-blind, randomized, placebo-controlled 3-arm trial of 121 HIV-infected participants on suppressive ART for >48 weeks, we evaluated the effects of 12 weeks of daily aspirin 100 mg, aspirin 300 mg, or placebo on soluble and cellular immune activation markers, flow-mediated dilation (FMD) of the brachial artery, and serum thromboxane B2, a direct readout of platelet COX-1 inhibition. Results The 300-mg and 100-mg aspirin arms did not differ from placebo in effects on soluble CD14, interleukin (IL)-6, soluble CD163, D-dimer, T-cell or monocyte activation, or the other immunologic endpoints measured. Endothelial function, as measured by FMD, also was not significantly changed when comparing the 300-mg and 100-mg aspirin arms to placebo. Conclusions Aspirin treatment for 12 weeks does not have a major impact on soluble CD14, IL-6, soluble CD163, D-dimer, T-cell or monocyte activation, or FMD, suggesting that inhibition of COX-1-mediated platelet activation does not significantly improve HIV-related immune activation and endothelial dysfunction. Although future studies are needed to further identify the causes and consequences of platelet activation in ART-treated HIV infection, interventions other than COX-1 inhibition will need to be explored to directly reduce immune activation in treated HIV infection.


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.


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