scholarly journals Delayed Blood Processing Leads to Rapid Deterioration in the Measurement of the Neutrophil Respiratory Burst by the Dihydrorhodamine‐123 Reduction Assay

2019 ◽  
Vol 96 (5) ◽  
pp. 389-396 ◽  
Author(s):  
Alex Quach ◽  
Shannon Glowik ◽  
Trishni Putty ◽  
Antonio Ferrante
Keyword(s):  
Respiratory Burst ◽  
Rapid Deterioration ◽  
Blood Processing ◽  
Dihydrorhodamine 123 ◽  
Reduction Assay ◽  
Neutrophil Respiratory Burst

Limitations on the use of dihydrorhodamine 123 for flow cytometric analysis of the neutrophil respiratory burst

1996 ◽  
Vol 191 (2) ◽  
pp. 187-196 ◽  
Author(s):  
L.J. van Pelt ◽  
R. van Zwieten ◽  
R.S. Weening ◽  
D. Roos ◽  
A.J. Verhoeven ◽  
...  
Keyword(s):  
Respiratory Burst ◽  
Flow Cytometric Analysis ◽  
Flow Cytometric ◽  
Dihydrorhodamine 123 ◽  
Neutrophil Respiratory Burst

scholarly journals Proton stoichiometry associated with human neutrophil respiratory-burst reactions.

1984 ◽  
Vol 259 (21) ◽  
pp. 13166-13171
Author(s):  
T G Gabig ◽  
B A Lefker ◽  
P J Ossanna ◽  
S J Weiss
Keyword(s):  
Respiratory Burst ◽  
Human Neutrophil ◽  
Neutrophil Respiratory Burst

scholarly journals Outbreaks of Mycobacterium tuberculosis MDR strains differentially induce neutrophil respiratory burst involving lipid rafts, p38 MAPK and Syk

2014 ◽  
Vol 14 (1) ◽  
Author(s):  
María Mercedes Romero ◽  
Juan Ignacio Basile ◽  
Beatriz López ◽  
Viviana Ritacco ◽  
Lucía Barrera ◽  
...  
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Lipid Rafts ◽  
P38 Mapk ◽  
Respiratory Burst ◽  
Neutrophil Respiratory Burst

fMLP-stimulated release of reactive oxygen species from adherent leukocytes increases microvessel permeability

2006 ◽  
Vol 290 (1) ◽  
pp. H365-H372 ◽  
Author(s):  
Longkun Zhu ◽  
Pingnian He
Keyword(s):  
Reactive Oxygen Species ◽  
Respiratory Burst ◽  
Leukocyte Adhesion ◽  
Autologous Blood ◽  
Blood Perfusion ◽  
Oxygen Species ◽  
Tnf Α ◽  
Microvessel Permeability ◽  
Adherent Leukocytes ◽  
Neutrophil Respiratory Burst

Our previous study ( Am J Physiol Heart Circ Physiol 288: H1331–H1338, 2005) demonstrated that TNF-α induced significant leukocyte adhesion without causing increases in microvessel permeability, and that formyl-Met-Leu-Phe-OH (fMLP)-stimulated neutrophils in the absence of adhesion increased microvessel permeability via released reactive oxygen species (ROS). The objective of our present study is to investigate the mechanisms that regulate neutrophil respiratory burst and the roles of fMLP-stimulated ROS release from adherent leukocytes in microvessel permeability. A technique that combines single-microvessel perfusion with autologous blood perfusion was employed in venular microvessels of rat mesenteries. Leukocyte adhesion was induced by systemic application of TNF-α. Microvessel permeability was assessed by measuring hydraulic conductivity ( Lp). The 2-h autologous blood perfusion after TNF-α application increased leukocyte adhesion from 1.2 ± 0.2 to 13.3 ± 1.6 per 100 μm of vessel length without causing increases in Lp. When fMLP (10 μM) was applied to either perfusate ( n = 5) or superfusate ( n = 8) in the presence of adherent leukocytes, Lptransiently increased to 4.9 ± 0.9 and 4.4 ± 0.3 times the control value, respectively. Application of superoxide dismutase or an iron chelator, deferoxamine mesylate, after fMLP application prevented or attenuated the Lpincrease. Chemiluminescence measurements in isolated neutrophils demonstrated that TNF-α alone did not induce ROS release but that preexposure of neutrophils to TNF-α in vivo or in vitro potentiated fMLP-stimulated ROS release. These results suggest a priming role of TNF-α in fMLP-stimulated neutrophil respiratory burst and indicate that the released ROS play a key role in leukocyte-mediated permeability increases during acute inflammation.

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