A Method for quantifying F-Actin in chemotactic peptide activated neutrophils: Study of the effect of tBOC peptide

Cell Motility ◽  
1985 ◽  
Vol 5 (6) ◽  
pp. 545-557 ◽  
Author(s):  
Thomas H. Howard ◽  
C. O. Oresajo
Keyword(s):  
Chemotactic Peptide ◽  
Activated Neutrophils

Inositol phosphate formation in chemotactic peptide-activated neutrophils obtained from normal and schizophrenic subjects

1989 ◽  
Vol 17 (4) ◽  
pp. 709-710 ◽  
Author(s):  
INDRAJIT DAS ◽  
JACQUELINE DE BELLEROCHE ◽  
ANTHONY G. JOLLEY ◽  
MOHAMMED A. ESSALI ◽  
STEVEN R. HIRSCH
Keyword(s):  
Inositol Phosphate ◽  
Chemotactic Peptide ◽  
Activated Neutrophils

Resting and stimulated cytosolic free calcium levels in neutrophils from patients with Bartter's syndrome

1987 ◽  
Vol 72 (4) ◽  
pp. 483-488 ◽  
Author(s):  
Francesco Di Virgilio ◽  
Lorenzo Calò ◽  
Salvatore Cantaro ◽  
Silvana Favaro ◽  
Antonio Piccoli ◽  
...  
Keyword(s):  
Free Calcium ◽  
Healthy Controls ◽  
Bartter’S Syndrome ◽  
Bartter's Syndrome ◽  
Chemotactic Peptide ◽  
Cytosolic Free Calcium ◽  
Fluorescent Indicator ◽  
Activated Neutrophils ◽  
Normal Controls

1. Cytosolic free calcium concentrations ([a2+]i) were measured in resting and chemotactic peptide-activated neutrophils from eight patients with Bartter's syndrome and compared with levels determined in neutrophils isolated from healthy controls. 2. [Ca2+]i was measured with the intracellular trappable fluorescent indicator Quin2. The synthetic tripeptide formylmethionyl-leucyl-phenylalanine (fMet-Leu-Phe) was used as a stimulant. 3. No difference was found in resting [Ca2+]i between neutrophils from normal controls and those from patients with Bartter's syndrome. 4. On the contrary increases in [Ca2+]i stimulated by fMet-Leu-Phe concentrations higher than 10−8 mol/l were significantly less in neutrophils from patients with Bartter's syndrome. 5. It is suggested that neutrophils from patients affected by Bartter's syndrome exhibit an intrinsic anomaly in the mechanism responsible for intracellular Ca2+ mobilization.

Anaphylatoxin and chemotactic peptide

2006 ◽  
pp. S15-S16
Author(s):  
S P H Alexander ◽  
A Mathie ◽  
J A Peters
Keyword(s):  
Chemotactic Peptide

Localization of Abscess with an Iodinated Synthetic Chemotactic Peptide

1982 ◽  
Vol 21 (03) ◽  
pp. 110-113 ◽  
Author(s):  
M.-S. Jiang ◽  
E. G. Corley ◽  
H. N. Wagner ◽  
M.-F. Tsan
Keyword(s):  
Chemotactic Peptide ◽  
Hatte Eine

N-Formyl Nle-Leu-Phe-Nle-Tyr-Lys ist ein wirksames synthetisches chemotaktisches Peptid (CP), welches sich mit hoher Affinität an chemotaktische Rezeptoren von neutrophilen Leukozyten bindet. Da das Peptid einen Tyrosin-Anteil enthält, kann es leicht mit radioaktivem Jod markiert werden. In dieser Arbeit haben wir die Möglichkeit der Abszeß-Lokalisierung durch intravenöse Gabe von radioaktivem CP untersucht. Das Peptid wurde nach der Chloramin-T-Methode mit 125J markiert und mittels Bio-Gel-P-2-Chromatographie gereinigt. Die endgültige Lösung hatte eine Reinheit von 88.5 ± 3.8% (n = 6) und eine spezifische Aktivität von 600-800 Ci/mM. Das jodierte CP zeigte eine spezifische Bindung an neutrophile Leukozyten des Kaninchens; die Anlagerung konnte durch nicht-markiertes CP verhindert werden. Nach Injektion von 4-6 ng 125J-CP/kg Körpergewicht in Kaninchen mit experimentellen Abszessen fand eine vorübergehende Neutropenie statt, gefolgt von einer Rebound-Neutrophilie. Das Verhältnis Abszeß zu Muskel (A/M) war 11.6 ± 1.1 nach 6 Std. und 11.0 ± 4.7 nach 24 Std., während das Verhältnis Abszeß zu Blut (A/B) 0.9 ± 0.2 nach 6 Std. und 3.7 ± 0.6, 24 Std. nach der Injektion war. Kontrolltiere, injiziert mit 125J, wiesen ein A/M-Verhältnis von 2.9 ± 0.2 und A/B-Verhältnis von 0.9 ± 0.3, 6 Std. nach der Injektion auf. Die Analyse der Radioaktivität im Blut nach 125J-CP-Gabe zeigte, daß der überwiegende Anteil (> 87%) als 125J-CP in der Plasmafraktion vorhanden war. Unsere Resultate geben Anlaß zur Vermutung, daß Radiojod-markiertes, synthetisches CP ein geeignetes Agens zur Abszeßlokalisierung sein kann. Allerdings ist eine weitere Verfeinerung der Methode notwendig.

Neutrophil Derived Cathepsin G Induces Potentially Thrombogenic Changes in Human Endothelial Cells: a Scanning Electron Microscopy Study in Static and Dynamic Conditions

1994 ◽  
Vol 72 (01) ◽  
pp. 140-145 ◽  
Author(s):  
Valeri Kolpakov ◽  
Maria Cristina D'Adamo ◽  
Lorena Salvatore ◽  
Concetta Amore ◽  
Alexander Mironov ◽  
...  
Keyword(s):  
Electron Microscopy ◽  
Scanning Electron Microscopy ◽  
Extracellular Matrix ◽  
Endothelial Cells ◽  
Thrombus Formation ◽  
Cathepsin G ◽  
Arterial Segment ◽  
Dynamic Conditions ◽  
Activated Neutrophils ◽  
Scanning Electron

SummaryActivated neutrophils may promote thrombus formation by releasing proteases which may activate platelets, impair the fibrinolytic balance and injure the endothelial monolayer.We have investigated the morphological correlates of damage induced by activated neutrophils on the vascular wall, in particular the vascular injury induced by released cathepsin G in both static and dynamic conditions.Human umbilical vein endothelial cells were studied both in a cell culture system and in a model of perfused umbilical veins. At scanning electron microscopy, progressive alterations of the cell monolayer resulted in cell contraction, disruption of the intercellular contacts, formation of gaps and cell detachment.Contraction was associated with shape change of the endothelial cells, that appeared star-like, while the underlying extracellular matrix, a potentially thrombogenic surface, was exposed. Comparable cellular response was observed in an “in vivo” model of perfused rat arterial segment. Interestingly, cathepsin G was active at lower concentrations in perfused vessels than in culture systems. Restoration of blood flow in the arterial segment previously damaged by cathepsin G caused adhesion and spreading of platelets on the surface of the exposed extracellular matrix. The subsequent deposition of a fibrin network among adherent platelets, could be at least partially ascribed to the inhibition by cathepsin G of the vascular fibrinolytic potential.This study supports the suggestion that the release of cathepsin G by activated neutrophils, f.i. during inflammation, may contribute to thrombus formation by inducing extensive vascular damage.

Nitric Oxide in Life and Death of Neutrophils

2019 ◽  
Vol 26 (31) ◽  
pp. 5764-5780 ◽  
Author(s):  
Svetlana I. Galkina ◽  
Ekaterina A. Golenkina ◽  
Galina M. Viryasova ◽  
Yulia M. Romanova ◽  
Galina F. Sud’ina
Keyword(s):  
Nitric Oxide ◽  
Cell Damage ◽  
Protective Role ◽  
Neutrophil Apoptosis ◽  
High Biological Activity ◽  
Life And Death ◽  
Signalling Molecule ◽  
Activated Neutrophils ◽  
Cell Death Mechanisms ◽  
Prostacyclin Synthase

Background: Nitric Oxide (NO) is a key signalling molecule that has an important role in inflammation. It can be secreted by endothelial cells, neutrophils, and other cells, and once in circulation, NO plays important roles in regulating various neutrophil cellular activities and fate. Objective: To describe neutrophil cellular responses influenced by NO and its concomitant compound peroxynitrite and signalling mechanisms for neutrophil apoptosis. Methods: Literature was reviewed to assess the effects of NO on neutrophils. Results: NO plays an important role in various neutrophil cellular activities and interaction with other cells. The characteristic cellular activities of neutrophils are adhesion and phagocytosis. NO plays a protective role in neutrophil-endothelial interaction by preventing neutrophil adhesion and endothelial cell damage by activated neutrophils. NO suppresses neutrophil phagocytic activity but stimulates longdistance contact interactions through tubulovesicular extensions or cytonemes. Neutrophils are the main source of superoxide, but NO flow results in the formation of peroxynitrite, a compound with high biological activity. Peroxynitrite is involved in the regulation of eicosanoid biosynthesis and inhibits endothelial prostacyclin synthase. NO and peroxynitrite modulate cellular 5-lipoxygenase activity and leukotriene synthesis. Long-term exposure of neutrophils to NO results in the activation of cell death mechanisms and neutrophil apoptosis. Conclusion: Nitric oxide and the NO/superoxide interplay fine-tune mechanisms regulating life and death in neutrophils.

Cytoplasmic pH regulation in phorbol ester-activated human neutrophils

1986 ◽  
Vol 251 (1) ◽  
pp. C55-C65 ◽  
Author(s):  
S. Grinstein ◽  
W. Furuya
Keyword(s):  
Metabolic Pathways ◽  
Phorbol Esters ◽  
Ph Regulation ◽  
Human Neutrophils ◽  
Hexose Monophosphate ◽  
Cytoplasmic Ph ◽  
Extracellular Acidification ◽  
Hexose Monophosphate Shunt ◽  
Activated Neutrophils ◽  
Cytoplasmic Acidification

Activation of neutrophils by 12-O-tetradecanoylphorbol-13-acetate (TPA) is accompanied by an initial cytoplasmic acidification, followed by an alkalinizing phase due to Na+-H+ countertransport. The source of the acidification, which is fully expressed by activation with TPA in Na+-free or amiloride-containing media, was investigated. The acidification phase was detected also in degranulated and enucleated cytoplasts, ruling out a major contribution by the nucleus or secretory vesicles. Cytoplasmic acidification was found to be associated with an extracellular acidification, suggesting metabolic generation of H+. Two principal metabolic pathways are stimulated in activated neutrophils: the reduction of O2 by NADPH-oxidase and the hexose monophosphate shunt. A good correlation was found between the activity of these pathways and the changes in cytoplasmic pH. Inhibition of superoxide synthesis prevented the TPA-induced cytoplasmic acidification. Moreover, activation of the hexose monophosphate shunt with permeable NADPH-oxidizing agents (in the absence of TPA) also produced a cytoplasmic acidification. Cytoplasmic acidification was also elicited by exogenous diacylglycerol and by other beta-phorbol diesters, which are activators of the kinase, but not by unesterified phorbol or by alpha-phorbol diesters, which are biologically inactive. The results suggest that the cytoplasmic acidification induced by phorbol esters in neutrophils reflects accumulation of H+ liberated during the metabolic burst that follows activation.

scholarly journals High expression of neutrophil and monocyte CD64 with simultaneous lack of upregulation of adhesion receptors CD11b, CD162, CD15, CD65 on neutrophils in severe COVID-19

2021 ◽  
Vol 8 ◽  
pp. 204993612110340
Author(s):  
Malgorzata Karawajczyk ◽  
Lena Douhan Håkansson ◽  
Miklos Lipcsey ◽  
Michael Hultström ◽  
Karlis Pauksens ◽  
...  
Keyword(s):  
Adhesion Molecules ◽  
Mean Fluorescence Intensity ◽  
Immune Dysfunction ◽  
Severe Form ◽  
Receptor Expression ◽  
Future Research ◽  
Early Biomarkers ◽  
Severe Stage ◽  
Activated Neutrophils ◽  
Edta Blood

Background and Aims: The pronounced neutrophilia observed in patients with coronavirus disease 2019 (COVID-19) infections suggests a role for these leukocytes in the pathology of the disease. Monocyte and neutrophil expression of CD64 and CD11b have been reported as early biomarkers to detect infections. The aim of this study was to study the expression of receptors for IgG (CD64) and adhesion molecules (CD11b, CD15s, CD65, CD162, CD66b) on neutrophils and monocytes in patients with severe COVID-19 after admission to an intensive care unit (ICU). Methods: The expression of receptors was analyzed using flow cytometry. EDTA blood from 23 patients with confirmed COVID-19 infection was sampled within 48 h of admission to the ICU. Leukocytes were labeled with antibodies to CD11b, CD15s, CD65s, CD162, CD64, and CD66b. Expression of receptors was reported as mean fluorescence intensity (MFI) or the percentage of cells expressing receptors. Results: Results are presented as comparison of COVID-19 patients with the healthy group and the receptor expression as MFI. Neutrophil receptors CD64 (2.5 versus 0.5) and CD66b (44.5 versus 34) were increased and CD15 decreased (21.6 versus 28.3) when CD65 (6.6 versus 4.4), CD162 (21.3 versus 21.1) and CD11b (10.5 versus 12) were in the same range. Monocytes receptors CD64 (30.5 versus 16.6), CD11b (18.7 versus 9.8), and CD162 (38.6 versus 36.5) were increased and CD15 decreased (10.3 versus 17.9); CD65 were in the same range (2.3 versus 1.96). Conclusion: Monocytes and neutrophils are activated during severe COVID-19 infection as shown by strong upregulation of CD64. High monocyte and neutrophil CD64 can be an indicator of a severe form of COVID19. The adhesion molecules (CD11b, CD162, CD65, and CD15) are not upregulated on otherwise activated neutrophils, which might lead to relative impairment of tissue migration. Low adhesion profile of neutrophils suggests immune dysfunction of neutrophils. Monocytes maintain upregulation of some adhesion molecules (CD11b, CD162) suggesting the persistence of an increased ability to migrate into tissues, even during a severe stage of COVID-19. Future research should focus on CD64 and CD11b kinetics in the context of prognosis.

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