Determinants of Neutrophil Adhesion Following Ischemia

1992 ◽  
pp. 57-69
Author(s):  
T. F. Lindsay ◽  
J. Hill ◽  
H. B. Hechtman
Keyword(s):  
Neutrophil Adhesion

scholarly journals High-Fat Diet Enhances Neutrophil Adhesion in LDLR-Null Mice Via Hypercitrullination of Histone H3

2021 ◽  
Author(s):  
Mizuko Osaka ◽  
Michiyo Deushi ◽  
Jiro Aoyama ◽  
Tomoko Funakoshi ◽  
Akihito Ishigami ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Histone H3 ◽  
Neutrophil Adhesion ◽  
High Fat

ICAM-1-independent adhesion of neutrophils to phorbol ester-stimulated human airway epithelial cells

1999 ◽  
Vol 277 (3) ◽  
pp. L465-L471 ◽  
Author(s):  
Alessandro Celi ◽  
Silvana Cianchetti ◽  
Stefano Petruzzelli ◽  
Stefano Carnevali ◽  
Filomena Baliva ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Airway Epithelial Cells ◽  
Bronchial Epithelial Cells ◽  
Neutrophil Adhesion ◽  
Late Time ◽  
Airway Epithelial ◽  
Bronchial Epithelial ◽  
Human Airway ◽  
Stimulation Of ◽  
Human Airway Epithelial Cells

Intercellular adhesion molecule-1 (ICAM-1) is the only inducible adhesion receptor for neutrophils identified in bronchial epithelial cells. We stimulated human airway epithelial cells with various agonists to evaluate whether ICAM-1-independent adhesion mechanisms could be elicited. Phorbol 12-myristate 13-acetate (PMA) stimulation of cells of the alveolar cell line A549 caused a rapid, significant increase in neutrophil adhesion from 11 ± 3 to 49 ± 7% (SE). A significant increase from 17 ± 4 to 39 ± 6% was also observed for neutrophil adhesion to PMA-stimulated human bronchial epithelial cells in primary culture. Although ICAM-1 expression was upregulated by PMA at late time points, it was not affected at 10 min when neutrophil adhesion was already clearly enhanced. Antibodies to ICAM-1 had no effect on neutrophil adhesion. In contrast, antibodies to the leukocyte integrin β-chain CD18 totally inhibited the adhesion of neutrophils to PMA-stimulated epithelial cells. These results demonstrate that PMA stimulation of human airway epithelial cells causes an increase in neutrophil adhesion that is not dependent on ICAM-1 upregulation.

Neutrophil-dependent augmentation of PAF-induced vasoconstriction and albumin flux in coronary arterioles

1998 ◽  
Vol 275 (4) ◽  
pp. H1138-H1147 ◽  
Author(s):  
Qiaobing Huang ◽  
Mac Wu ◽  
Cynthia Meininger ◽  
Katherine Kelly ◽  
Yuan Yuan
Keyword(s):  
Platelet Activating Factor ◽  
Microvascular Dysfunction ◽  
Low Flow ◽  
Intercellular Adhesion Molecule ◽  
Neutrophil Adhesion ◽  
Intercellular Adhesion Molecule 1 ◽  
Apparent Permeability ◽  
Inflammatory Reactions ◽  
Coronary Arterioles ◽  
Flow Velocities

Platelet-activating factor (PAF) has been implicated in the pathogenesis of ischemic heart disease, reperfusion injury, and inflammatory reactions. Although neutrophils have been shown to primarily mediate PAF-induced microvascular dysfunction, the vasoactive effect of PAF and its neutrophil-dependent mechanism have not been directly and systematically studied in coronary resistance vessels. Therefore, the aim of this study was to examine the effects of PAF on coronary arteriolar function and neutrophil dynamics using an isolated and perfused microvessel preparation. Topical application of PAF to the vessels induced a dose-dependent decrease in the diameter but an increase in the apparent permeability coefficient of albumin. Disruption of the endothelium abolished the vasomotor response to PAF, and perfusion of neutrophils significantly augmented PAF-induced changes in vasomotor tone and permeability. Furthermore, the interaction between neutrophils and the endothelium was studied in the intact perfused coronary arterioles. Under control conditions, there were no adherent neutrophils observed in the vessels at varied intraluminal flow velocities. However, administration of PAF caused neutrophil adhesion to the endothelium of coronary arterioles at low flow velocities. Western blot analysis indicated that PAF upregulated the expression of intercellular adhesion molecule-1 in cultured coronary microvascular endothelial cells. Taken together, the results suggest that 1) PAF induces vasoconstriction and hyperpermeability in coronary arterioles via an endothelium-dependent and neutrophil-mediated mechanism, and 2) PAF is able to stimulate neutrophil adhesion in coronary arterioles under a condition of low flow rate.

A cooperation between bradykinin B2 and dopamine D2 receptors regulates neutrophil adhesion to endothelial cells

2017 ◽  
Vol 263 ◽  
pp. e76
Author(s):  
Anna Niewiarowska-Sendo ◽  
Agnieszka Polit ◽  
Anna Labedz-Maslowska ◽  
Andrzej Kozik ◽  
Ibeth Guevara-Lora
Keyword(s):  
Endothelial Cells ◽  
D2 Receptors ◽  
Dopamine D2 Receptors ◽  
Neutrophil Adhesion ◽  
Dopamine D2

Exposure of intestinal epithelial cell HT29 to bile acids and ammonia enhances Mac-1-mediated neutrophil adhesion

1999 ◽  
Vol 48 (5) ◽  
pp. 265-273 ◽  
Author(s):  
R. Miyata ◽  
K. Iwabuchi ◽  
S. Watanabe ◽  
N. Sato ◽  
I. Nagaoka
Keyword(s):  
Epithelial Cell ◽  
Bile Acids ◽  
Intestinal Epithelial Cell ◽  
Neutrophil Adhesion ◽  
Intestinal Epithelial

Abstract 596: Increased Migration of Neutrophils Across Endothelial Cells from Patients with Pulmonary Arterial Hypertension is Related to Reduced Platelet Endothelial Cell Adhesion Molecule -1 and is Prevented by the Neutrophil Elastase Inhibitor Elafin

2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Shalina Taylor ◽  
Jan-Renier Moonen ◽  
Kazuya Miyagawa ◽  
Mingxia Gu ◽  
Silin Sa ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Neutrophil Elastase ◽  
Cell Adhesion Molecule ◽  
Neutrophil Adhesion ◽  
Elastase Inhibitor ◽  
Platelet Endothelial Cell Adhesion ◽  
Pulmonary Arterial ◽  
And Control ◽  
Cell Adhesion Molecule 1 ◽  
Endothelial Cell Adhesion

Pulmonary arterial hypertension (PAH) is a devastating progressive disease associated with a high mortality despite current vasodilator therapies. Perivascular inflammation and high levels of neutrophil elastase are thought to play a pivotal role in the adverse vascular remodeling of small pulmonary arteries that causes PAH. Despite this, the function of neutrophils and in particular, their interaction with the pulmonary arterial endothelium has not been studied in PAH. We hypothesized that neutrophil functions such as adhesion to a substratum or to endothelial cells and transmigration across a substratum or trans-endothelial migration (TEM) are abnormal in PAH on the basis of dysfunction of both cell types. Using a neutrophil like cell line dHL-60 and isolated human neutrophils from donors and PAH patients, we demonstrated no significant difference in adhesion to PAH vs. control PAECs when stimulated with TNF-α (100μg/mL). However, TEM of both IL-8 (100ng/ml) and fMLP (100nM) stimulated dHL-60 cells and donor neutrophils was enhanced in PAH vs. control PAECs (p<0.01) likely related to reduced expression of Platelet Endothelial Cell Adhesion Molecule -1 (PECAM-1) in PAH PAECs (p <0.001). We therefore further hypothesized that inhibition of neutrophil elastase via recombinant human elafin would be sufficient to reverse TEM in both PAH and control PAEC by reducing neutrophil adhesion, a feature known to be elastase-dependent. Administration of elafin (1μg/mL) attenuated fMLP and IL-8 induced dHL-60 and neutrophil adhesion to fibrinogen and fibronectin (p<0.05 for both) as well as transmigration across both substrates (p<0.05 for both). Elafin reduced adhesion of neutrophil similarly in PAH and control PAEC (p <0.05 for both). Furthermore, in a dose dependent manner, elafin inhibited TEM in PAH PAEC by 40% in control PAECs, by 20% (p<0.001 and p<0.01 respectively) bringing values to within the same range of suppressing but not eliminating TEM. We therefore conclude that despite the reduction in PECAM-1 in PAH PAEC, inhibition of neutrophil adhesion with the elastase inhibitor elafin is sufficient to prevent the enhanced TEM. Elafin may therefore be of benefit in suppressing the deleterious impact of neutrophil in enhanced inflammation seen in PAH.

Association of Neutrophil Adhesion Molecules Expression and Change of sICAM-1 Concentration after Coronary Artery Stenting with Later Restenosis

2001 ◽  
Vol 31 (1) ◽  
pp. 45 ◽  
Author(s):  
Jin Su Hwang ◽  
Jei Keon Chae ◽  
Bang Ju La ◽  
Byung Hyun Rhee ◽  
Won Ho Kim ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Adhesion Molecules ◽  
Neutrophil Adhesion ◽  
Coronary Artery Stenting

Porcine endothelium activated by anti-??-GAL antibody binding mediates increased human neutrophil adhesion under flow

2003 ◽  
Vol 76 (7) ◽  
pp. 1112-1119 ◽  
Author(s):  
Cecilia Ehrnfelt ◽  
Lena Serrander ◽  
Jan Holgersson
Keyword(s):  
Human Neutrophil ◽  
Antibody Binding ◽  
Neutrophil Adhesion

Blockade of CD18-Dependent Neutrophil Adhesion Limits Myocardial Infarct Size Following Coronary Artery Occlusion in Cynomolgus Monkeys

1991 ◽  
pp. 298-298
Author(s):  
Raymond J. Winquist ◽  
P. Frei ◽  
M. McFarland ◽  
P. Harrison ◽  
G. Letts ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Infarct Size ◽  
Myocardial Infarct ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Neutrophil Adhesion ◽  
Myocardial Infarct Size ◽  
Cynomolgus Monkeys
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