Reactive oxygen product formation after Fcγ receptor-mediated neutrophil activation by monomeric mouse IgG2a: implications for the generation of first dose effects after OKT3 treatment

1993 ◽  
Vol 23 (4) ◽  
pp. 977-980 ◽  
Author(s):  
Gerhard J. Zlabinger ◽  
Alexander R. Rosenkranz ◽  
Sabine Schmaldienst ◽  
Karl Stuhlmeier ◽  
Georg Böhmig ◽  
...  
Keyword(s):  
Reactive Oxygen ◽  
Product Formation ◽  
Neutrophil Activation ◽  
Fcγ Receptor ◽  
Dose Effects ◽  
Mouse Igg2a

scholarly journals Role of TNF-α-induced reactive oxygen species in endothelial dysfunction during reperfusion injury

2008 ◽  
Vol 295 (6) ◽  
pp. H2242-H2249 ◽  
Author(s):  
Xue Gao ◽  
Hanrui Zhang ◽  
Souad Belmadani ◽  
Junxi Wu ◽  
Xiangbin Xu ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Endothelial Dysfunction ◽  
Myocardial Ischemia ◽  
Endothelial Function ◽  
Xanthine Oxidase ◽  
Reactive Oxygen ◽  
Neutrophil Activation ◽  
Superoxide Production ◽  
Oxygen Species ◽  
Tnf Α

We hypothesized that neutralization of TNF-α at the time of reperfusion exerts a salubrious role on endothelial function and reduces the production of reactive oxygen species. We employed a mouse model of myocardial ischemia-reperfusion (I/R, 30 min/90 min) and administered TNF-α neutralizing antibodies at the time of reperfusion. I/R elevated TNF-α expression (mRNA and protein), whereas administration of anti-TNF-α before reperfusion attenuated TNF-α expression. We detected TNF-α expression in vascular smooth muscle cells, mast cells, and macrophages, but not in the endothelial cells. I/R induced endothelial dysfunction and superoxide production. Administration of anti-TNF-α at the onset of reperfusion partially restored nitric oxide-mediated coronary arteriolar dilation and reduced superoxide production. I/R increased the activity of NAD(P)H oxidase and of xanthine oxidase and enhanced the formation of nitrotyrosine residues in untreated mice compared with shams. Administration of anti-TNF-α before reperfusion blocked the increase in activity of these enzymes. Inhibition of xanthine oxidase (allopurinol) or NAD(P)H oxidase (apocynin) improved endothelium-dependent dilation and reduced superoxide production in isolated coronary arterioles following I/R. Interestingly, I/R enhanced superoxide generation and reduced endothelial function in neutropenic animals and in mice treated with a neutrophil NAD(P)H oxidase inhibitor, indicating that the effects of TNF-α are not through neutrophil activation. We conclude that myocardial ischemia initiates TNF-α expression, which induces vascular oxidative stress, independent of neutrophil activation, and leads to coronary endothelial dysfunction.

Neutrophil activation by anti-β 2 glycoprotein I monoclonal antibodies via Fcγ receptor II

1995 ◽  
Vol 57 (3) ◽  
pp. 387-394 ◽  
Author(s):  
Josiane Arvieux ◽  
Marie-Christine Jacob ◽  
Bernard Roussel ◽  
Jean-Claude Bensa ◽  
Maurice G. Colomb
Keyword(s):  
Monoclonal Antibodies ◽  
Neutrophil Activation ◽  
Fcγ Receptor ◽  
Glycoprotein I

scholarly journals Reactive Oxygen Species and low-dose effects of tritium on bacterial cells

2019 ◽  
Vol 208-209 ◽  
pp. 106035 ◽  
Author(s):  
Tatiana V. Rozhko ◽  
Evdokiya I. Nogovitsyna ◽  
Gennady A. Badun ◽  
Aleksandra N. Lukyanchuk ◽  
Nadezhda S. Kudryasheva
Keyword(s):  
Reactive Oxygen Species ◽  
Low Dose ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Bacterial Cells ◽  
Dose Effects ◽  
Low Dose Effects

scholarly journals PTPN22 Is a Critical Regulator of Fcγ Receptor–Mediated Neutrophil Activation

2016 ◽  
Vol 197 (12) ◽  
pp. 4771-4779 ◽  
Author(s):  
Sonja Vermeren ◽  
Katherine Miles ◽  
Julia Y. Chu ◽  
Donald Salter ◽  
Rose Zamoyska ◽  
...  
Keyword(s):  
Neutrophil Activation ◽  
Fcγ Receptor

scholarly journals A new hydrophilic polysulfone hemodialysis membrane can prevent platelet–neutrophil interactions and successive neutrophil activation

2019 ◽  
Vol 42 (4) ◽  
pp. 175-181 ◽  
Author(s):  
Yoko Koga ◽  
Hiroyuki Meguro ◽  
Hiroaki Fujieda ◽  
Yoshiyuki Ueno ◽  
Keishi Miwa ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Blood Cells ◽  
Cell Activation ◽  
Molecular Mechanisms ◽  
Reactive Oxygen ◽  
Neutrophil Activation ◽  
Human Neutrophils ◽  
Oxygen Species ◽  
Polysulfone Membrane ◽  
Polysulfone Membranes

Purpose: Microaggregates have often been observed during hemodialysis and are clearly associated with complications of hemodialysis therapy. In this study, we aimed to clarify the effects of two polysulfone membranes, with different abilities to activate blood cells, on the formation of these microaggregates; we also investigated their molecular mechanisms. Methods: Human whole blood was circulated through a mini-module dialyzer using the membranes in vitro; platelet–neutrophil complexes in blood were determined by flow cytometry. Isolated human neutrophils were incubated with the membranes in plasma, in the presence or absence of platelets, followed by flow cytometric analysis of intracellular reactive oxygen species and cell-surface activated CD11b on neutrophils. Results: CX-U, a conventional polysulfone membrane with remarkable cell activation, induced the formation of platelet–neutrophil complexes; however, NV-U, a new hydrophilic polysulfone membrane with slight or no cell activation, did not cause complex formation. Moreover, CX-U-induced reactive oxygen species production and the increase in activated CD11b expression on neutrophils were enhanced by platelets. On the other hand, NV-U hardly affected neutrophil activation, regardless of whether platelets were present or not. The enhancement of CX-U-induced neutrophil activations by platelets was greatly inhibited by anti-CD62P antibody. Conclusion: The ability of polysulfone membranes to activate blood cells is closely related to platelet–neutrophil interaction. Therefore, a biocompatible membrane, like NV-U, can be expected to prevent microaggregate formation during hemodialysis and avoid subsequent cell activation.

Neutrophil activation and production of reactive oxygen species in pre-eclampsia

2003 ◽  
Vol 21 (2) ◽  
pp. 395-402 ◽  
Author(s):  
Virginia M Lee ◽  
Paulene A Quinn ◽  
Sonja C Jennings ◽  
Leong L Ng
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Neutrophil Activation ◽  
Oxygen Species

scholarly journals Interaction of Poliovirus with Its Receptor Affords a High Level of Infectivity to the Virion in Poliovirus Infections Mediated by the Fc Receptor

1999 ◽  
Vol 73 (2) ◽  
pp. 1066-1074 ◽  
Author(s):  
Minetaro Arita ◽  
Hitoshi Horie ◽  
Mineo Arita ◽  
Akio Nomoto
Keyword(s):  
Monoclonal Antibodies ◽  
Conformational Change ◽  
Specific Interaction ◽  
Fcγ Receptor ◽  
High Affinity ◽  
Poliovirus Infection ◽  
L Cells ◽  
Poliovirus Receptor ◽  
High Level ◽  
Mouse Igg2a

ABSTRACT Poliovirus infects susceptible cells through the poliovirus receptor (PVR), which functions to bind virus and to change its conformation. These two activities are thought to be necessary for efficient poliovirus infection. How binding and conformation conversion activities contribute to the establishment of poliovirus infection was investigated. Mouse L cells expressing mouse high-affinity Fcγ receptor molecules were established and used to study poliovirus infection mediated by mouse antipoliovirus monoclonal antibodies (MAbs) (immunoglobulin G2a [IgG2a] subtypes) or PVR-IgG2a, a chimeric molecule consisting of the extracellular moiety of PVR and the hinge and Fc portion of mouse IgG2a. The antibodies and PVR-IgG2a showed the same degree of affinity for poliovirus, but the infectivities mediated by these molecules were different. Among the molecules tested, PVR-IgG2a mediated the infection most efficiently, showing 50- to 100-fold-higher efficiency than that attained with the different MAbs. A conformational change of poliovirus was induced only by PVR-IgG2a. These results strongly suggested that some specific interaction(s) between poliovirus and the PVR is required for high-level infectivity of poliovirus in this system.

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