Constitutive production of PAI-II and increased surface expression of GM1 ganglioside by peripheral blood monocytes from patients with AIDS: evidence of monocyte activation in vivo

1992 ◽  
Vol 52 (3) ◽  
pp. 282-286 ◽  
Author(s):  
Dominick L. Auci ◽  
Seto M. Chice ◽  
Helen G. Durkin ◽  
Mandakolathur R. Murali
Keyword(s):  
Peripheral Blood ◽  
Surface Expression ◽  
Gm1 Ganglioside ◽  
Blood Monocytes ◽  
Monocyte Activation ◽  
Peripheral Blood Monocytes ◽  
Constitutive Production

Is the Success of Cefazolin plus Ertapenem in Methicillin-Susceptible Staphylococcus aureus Bacteremia Based on Release of Interleukin 1-beta?

2022 ◽  
Author(s):  
Dan Smelter ◽  
Mary Hayney ◽  
George Sakoulas ◽  
Warren Rose
Keyword(s):  
Staphylococcus Aureus ◽  
Peripheral Blood ◽  
Interleukin 1 ◽  
Interleukin 1 Beta ◽  
Blood Monocytes ◽  
Salvage Regimen ◽  
Peripheral Blood Monocytes ◽  
Staphylococcus Aureus Bacteremia

Cefazolin and ertapenem has been shown to be an effective salvage regimen for refractory methicillin-susceptible Staphylococcus aureus bacteremia. Our findings suggest cefazolin plus ertapenem in vitro stimulates interleukin-1β release from peripheral blood monocytes both with and without S. aureus presence. This IL-1β augmentation was primarily driven by ertapenem. These findings support further exploration of cefazolin plus ertapenem in MSSA bacteremia and may partially explain its marked potency in vivo despite modest synergy in vitro .

scholarly journals AP-1 (Activated Protein-1) Transcription Factor JunD Regulates Ischemia/Reperfusion Brain Damage via IL-1β (Interleukin-1β)

Stroke ◽  
2019 ◽  
Vol 50 (2) ◽  
pp. 469-477 ◽  
Author(s):  
Candela Diaz-Cañestro ◽  
Martin F. Reiner ◽  
Nicole R. Bonetti ◽  
Luca Liberale ◽  
Mario Merlini ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Brain Injury ◽  
Acute Ischemic Stroke ◽  
Peripheral Blood ◽  
Ischemia Reperfusion ◽  
Interleukin 1Β ◽  
Blood Monocytes ◽  
Peripheral Blood Monocytes

Background and Purpose— Inflammation is a major pathogenic component of ischemia/reperfusion brain injury, and as such, interventions aimed at inhibiting inflammatory mediators promise to be effective strategies in stroke therapy. JunD—a member of the AP-1 (activated protein-1) family of transcription factors—was recently shown to regulate inflammation by targeting IL (interleukin)-1β synthesis and macrophage activation. The purpose of the present study was to assess the role of JunD in ischemia/reperfusion-induced brain injury. Methods— WT (wild type) mice randomly treated with either JunD or scramble (control) siRNA were subjected to 45 minutes of transient middle cerebral artery occlusion followed by 24 hours of reperfusion. Stroke size, neurological deficit, plasma/brain cytokines, and oxidative stress determined by 4-hydroxynonenal immunofluorescence staining were evaluated 24 hours after reperfusion. Additionally, the role of IL-1β was investigated by treating JunD siRNA mice with an anti–IL-1β monoclonal antibody on reperfusion. Finally, JunD expression was assessed in peripheral blood monocytes isolated from patients with acute ischemic stroke. Results— In vivo JunD knockdown resulted in increased stroke size, reduced neurological function, and increased systemic inflammation, as confirmed by higher neutrophil count and lymphopenia. Brain tissue IL-1β levels were augmented in JunD siRNA mice as compared with scramble siRNA, whereas no difference was detected in IL-6, TNF-α (tumor necrosis factor-α), and 4-hydroxynonenal levels. The deleterious effects of silencing of JunD were rescued by treating mice with an anti–IL-1β antibody. In addition, JunD expression was decreased in peripheral blood monocytes of patients with acute ischemic stroke at 6 and 24 hours after onset of stroke symptoms compared with sex- and age-matched healthy controls. Conclusions— JunD blunts ischemia/reperfusion-induced brain injury via suppression of IL-1β.

nef-deleted HIV-1 inhibits phagocytosis by monocyte-derived macrophages in vitro but not by peripheral blood monocytes in vivo

AIDS ◽  
2001 ◽  
Vol 15 (8) ◽  
pp. 945-955 ◽  
Author(s):  
Katherine Kedzierska ◽  
Johnson Mak ◽  
Anthony Jaworowski ◽  
Alison Greenway ◽  
Antoniette Violo ◽  
...  
Keyword(s):  
Peripheral Blood ◽  
Blood Monocytes ◽  
Peripheral Blood Monocytes ◽  
Hiv 1

Validation of the Circulating Monocyte Being Representative of the Cholesterol-Loaded Macrophage: Biomediator Activity

2008 ◽  
Vol 132 (9) ◽  
pp. 1432-1435
Author(s):  
Sridevi Devaraj ◽  
Ishwarlal Jialal
Keyword(s):  
Peripheral Blood ◽  
Superoxide Anion ◽  
Interleukin 1 ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Surface Expression ◽  
Blood Monocytes ◽  
Peripheral Blood Monocytes ◽  
Macrophage Activity ◽  
Human Endothelium

Abstract Context.—Inflammation is pivotal to atherosclerosis. The monocyte-macrophage, a crucial cell in atherogenesis, is present during all stages of atherosclerosis. However, there is a paucity of data comparing circulating monocytes to cholesterol-laden macrophages (foam cells), with regard to their atherogenic properties, especially in subjects with established risk factors such as hyperlipidemia. Objective.—To determine whether the circulating blood monocyte is representative of the cholesterol-loaded macrophage with regard to its proatherogenicity in healthy controls and hyperlipidemic patients. Design.—Fasting blood was drawn from 32 subjects (n = 16 controls and n = 16 hyperlipidemic patients), and peripheral blood monocytes were obtained. Also, macrophages were cultured and loaded with acetyl low-density lipoprotein on day 10. Day 1 peripheral blood monocytes and day 11 cholesterol-loaded macrophages were assessed for release of superoxide anion and cytokines (interleukin 1, interleukin 6, tumor necrosis factor α); surface expression of CD11b, VLA-4, and CD40; and adhesion to human endothelium. Results.—Monocyte and cholesterol-loaded macrophage superoxide anion release, cytokines, and adhesion of monocytes to human endothelium were significantly increased in hyperlipidemic patients compared with controls. Furthermore, following cholesterol loading, there were no significant differences in monocyte versus cholesterol-loaded macrophage activity (P = .71). Also, CD14 and CD11b surface expression on monocytes was significantly increased in hyperlipidemic patients as compared with controls. The magnitude of change in the monocytes versus cholesterol-loaded macrophages was similar. Conclusions.—From these studies, we can conclude that the monocyte, which is readily accessible, is an appropriate cell to study for modulation of proatherogenic activity, especially with regard to genomic and proteomic analyses/ microarrays.

scholarly journals Cellular microRNA expression correlates with susceptibility of monocytes/macrophages to HIV-1 infection

Blood ◽  
2009 ◽  
Vol 113 (3) ◽  
pp. 671-674 ◽  
Author(s):  
Xu Wang ◽  
Li Ye ◽  
Wei Hou ◽  
Yu Zhou ◽  
Yan-Jian Wang ◽  
...  
Keyword(s):  
Peripheral Blood ◽  
Direct Evidence ◽  
Differential Susceptibility ◽  
Blood Monocytes ◽  
Peripheral Blood Monocytes ◽  
Monocytes And Macrophages ◽  
Anti Hiv ◽  
Hiv 1

AbstractAlthough both monocytes and macrophages possess essential requirements for HIV-1 entry, peripheral blood monocytes are infrequently infected with HIV-1 in vivo and in vitro. In contrast, tissue macrophages and monocyte-derived macrophages in vitro are highly susceptible to infection with HIV-1 R5 tropic strains. We investigated intracellular anti–HIV-1 factors that contribute to differential susceptibility of monocytes/macrophages to HIV-1 infection. Freshly isolated monocytes from peripheral blood had significantly higher levels of the anti–HIV-1 microRNAs (miRNA, miRNA-28, miRNA-150, miRNA-223, and miRNA-382) than monocyte-derived macrophages. The suppression of these anti–HIV-1 miRNAs in monocytes facilitates HIV-1 infectivity, whereas increase of the anti–HIV-1 miRNA expression in macrophages inhibited HIV-1 replication. These findings provide compelling and direct evidence at the molecular level to support the notion that intracellular anti–HIV-1 miRNA-mediated innate immunity may have a key role in protecting monocytes/macrophages from HIV-1 infection.

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