Production of hydrogen peroxide by peripheral blood monocytes and specific macrophages during experimental infection with Trypanosoma cruzi in vivo

2003 ◽  
Vol 27 (10) ◽  
pp. 853-861 ◽  
Author(s):  
R Melo
Keyword(s):  
Hydrogen Peroxide ◽  
Trypanosoma Cruzi ◽  
Experimental Infection ◽  
Peripheral Blood ◽  
Blood Monocytes ◽  
Peripheral Blood Monocytes ◽  
Production Of Hydrogen

scholarly journals Increased production of hydrogen peroxide by peripheral blood monocytes associated with smoking exposure intensity in smokers

2012 ◽  
Vol 9 (1) ◽  
pp. 45 ◽  
Author(s):  
Suzana E Tanni ◽  
Camila R Correa ◽  
Aparecida Y Angeleli ◽  
Simone A Vale ◽  
Liana S Coelho ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Peripheral Blood ◽  
Blood Monocytes ◽  
Peripheral Blood Monocytes ◽  
Smoking Exposure ◽  
Production Of Hydrogen

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

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.

scholarly journals Generation of Feline Dendritic Cells Derived from Peripheral Blood Monocytes for In Vivo Use

2005 ◽  
Vol 12 (10) ◽  
pp. 1202-1208 ◽  
Author(s):  
Giulia Freer ◽  
Donatella Matteucci ◽  
Paola Mazzetti ◽  
Leonia Bozzacco ◽  
Mauro Bendinelli
Keyword(s):  
Immune Response ◽  
Dendritic Cells ◽  
Peripheral Blood ◽  
Poly I:C ◽  
Interleukin 4 ◽  
Blood Monocytes ◽  
Autologous Plasma ◽  
Peripheral Blood Monocytes

ABSTRACT Dendritic cells (DCs) are professional antigen-presenting cells that can prime T cells and polarize the cellular immune response. Because Th1-type immune responses have been connected to success in combating viral infection, a promising therapeutic application of DCs would be their differentiation in vitro and injection back into the host to boost an immune response in infected animals. This study was aimed both at developing a protocol to cultivate feline DCs in the absence of exogenous proteins for their use in vivo and at investigating what might be the most appropriate stimulus to induce their maturation in vitro and finding correlates of maturation. We generated DCs from peripheral blood monocytes in the presence of feline interleukin-4 and granulocyte-macrophage colony stimulating factor, and after 5 days their maturation was induced with either lipopolysaccharide, human recombinant tumor necrosis factor alpha, poly(I:C), or activated feline platelets. After 48 h, their CD14, CD1a, major histocompatibility complex class II, and B7.1 surface expression was analyzed in parallel with their ability to uptake antigen or prime a mixed leukocyte reaction. The results presented show that feline DCs cultured in autologous plasma differentiate and are able to mature in the presence of stimuli similar to the ones currently used for other species. The present work sets the grounds for future use of DCs obtained by the protocol described for in vivo vaccination and immunotherapy of feline immunodeficiency virus-infected cats.

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