The kinetics of E-selectin- and P-selectin-induced intermediate activation of integrin αLβ2 on neutrophils

2021 ◽  
Vol 134 (18) ◽  
Author(s):  
Fangyuan Zhou ◽  
Fang Zhang ◽  
Veronika I. Zarnitsyna ◽  
Larissa Doudy ◽  
Zhou Yuan ◽  
...  
Keyword(s):  
Room Temperature ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Slow Increase ◽  
Rolling Velocity ◽  
Dependent Change ◽  
Temperature Activation ◽  
Selectin Binding ◽  
Kinetics Of ◽  
Dose Dependent

ABSTRACT Selectins and integrins are key players in the adhesion and signaling cascade that recruits leukocytes to inflamed tissues. Selectin binding induces β2 integrin binding to slow leukocyte rolling. Here, a micropipette was used to characterize neutrophil adhesion to E-selectin and intercellular adhesion molecule-1 (ICAM-1) at room temperature. The time-dependent adhesion frequency displayed two-stage kinetics, with an E-selectin-mediated fast increase to a low plateau followed by a slow increase to a high plateau mediated by intermediate-affinity binding of integrin αLβ2 to ICAM-1. The αLβ2 activation required more than 5 s contact to E-selectin and spleen tyrosine kinase (Syk) activity. A multi-zone channel was used to analyze αLβ2 activation by P-selectin in separate zones of receptors or antibodies, finding an inverse relationship between the rolling velocity on ICAM-1 and P-selectin dose, and a P-selectin dose-dependent change from bent to extended conformations with a closed headpiece that was faster at 37°C than at room temperature. Activation of αLβ2 exhibited different levels of cooperativity and persistent times depending on the strength and duration of selectin stimulation. These results define the precise timing and kinetics of intermediate activation of αLβ2 by E- and P-selectins.

Molecular determinants of lipid mediator-induced leukocyte adherence and emigration in rat mesenteric venules

1994 ◽  
Vol 266 (3) ◽  
pp. H847-H853 ◽  
Author(s):  
B. J. Zimmerman ◽  
J. W. Holt ◽  
J. C. Paulson ◽  
D. C. Anderson ◽  
M. Miyasaka ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Platelet Activating Factor ◽  
Leukotriene B4 ◽  
Intercellular Adhesion Molecule ◽  
Lipid Mediator ◽  
Leukocyte Rolling ◽  
Leukocyte Adherence ◽  
Intercellular Adhesion Molecule 1 ◽  
Rolling Velocity ◽  
Molecular Determinants

The objective of this study was to identify the molecular determinants of leukocyte rolling, adherence, and emigration elicited in postcapillary venules by the lipid mediators leukotriene B4 (LTB4) or platelet-activating factor (PAF). Leukocyte-endothelial cell adhesion and shear rate were monitored in rat mesenteric venules during superfusion with either LTB4 or PAF in the presence or absence of monoclonal antibodies (MAbs) directed against either leukocyte (CD18, CD11b) or endothelial cell [intercellular adhesion molecule 1 (ICAM-1), E-selectin, P-selectin] adhesion glycoproteins. In untreated animals and in animals receiving a nonbinding control MAb, LTB4 and PAF increased the number of both adherent (8- and 4-fold, respectively) and emigrated (14- and 8-fold, respectively) leukocytes, while reducing leukocyte rolling velocity (36 and 33%, respectively). The LTB4- and PAF-induced leukocyte adherence and emigration were significantly attenuated by pretreatment with MAbs directed against CD18, CD11b, ICAM-1, and E-selectin, but not P-selectin. The reduction in leukocyte rolling velocity induced by LTB4 was not affected by any of the MAbs; however, both P- and E-selectin MAbs significantly attenuated the reduction in leukocyte rolling velocity elicited by PAF. The results of this study indicate that the leukocyte adherence and emigration induced by both LTB4 and PAF are mediated by CD11b/CD18 on leukocytes and by ICAM-1 and E-selectin on endothelial cells. The molecular determinant of leukocyte rolling appears to be mediator specific, with the selectins mediating the rolling elicited by PAF.

Regional differences in constitutive and induced ICAM-1 expression in vivo

1995 ◽  
Vol 269 (6) ◽  
pp. H1955-H1964 ◽  
Author(s):  
J. Panes ◽  
M. A. Perry ◽  
D. C. Anderson ◽  
A. Manning ◽  
B. Leone ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Regional Differences ◽  
Time Course ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Fourfold Increase ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Higher Doses

The aim of the present study was to characterize and compare the expression of intercellular adhesion molecule 1 (ICAM-1) on unstimulated and endotoxin-challenged endothelial cells in different tissues of the rat. ICAM-1 expression was measured using 125I-labeled anti-rat ICAM-1 monoclonal antibody (MAb) and an isotype-matched control MAb labeled with 131I (to correct for nonspecific accumulation of the binding MAb). Under baseline conditions, ICAM-1 MAb binding was observed in all organs. The binding of 125I-ICAM-1 MAb varied widely among organs, with the largest accumulation (per g tissue) in the lung, followed by heart (1/30th of lung activity), splanchnic organs (1/50th of lung activity), thymus (1/100th of lung activity), testes (1/300th of lung activity), and skeletal muscle (1/800th of lung activity). Endotoxin induced an increase in ICAM-1 MAb binding in all organs except the spleen. Endotoxin-induced upregulation of ICAM-1 was greatest in heart and skeletal muscle (5- to 10-fold), whereas the remaining organs exhibited a two- to fourfold increase in ICAM-1 expression. Maximal upregulation of ICAM-1 occurred at 9-12 h after endotoxin administration. A dose-dependent increase in ICAM-1 expression was elicited by 0.1-10 microgram/kg, with higher doses (up to 5 mg/kg) producing no further increment. Induction of ICAM-1 mRNA after endotoxin was observed in all tissues examined (lung, heart, intestine), peaked at 3 h, and then rapidly returned to control levels. These findings indicate that ICAM-1 is constitutively expressed on vascular endothelium in all organs of the rat and that there are significant regional differences in the magnitude and time course of endotoxin-induced ICAM-1 expression.

scholarly journals The Domain Structure of ICAM-1 and the Kinetics of Binding to Rhinovirus

1998 ◽  
Vol 72 (7) ◽  
pp. 6244-6246 ◽  
Author(s):  
José M. Casasnovas ◽  
Joanna K. Bickford ◽  
Timothy A. Springer
Keyword(s):  
Crystal Structures ◽  
Domain Structure ◽  
Adhesion Molecule ◽  
Extracellular Domain ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
X Ray ◽  
Kinetics Of

ABSTRACT Fragments of intercellular adhesion molecule 1 (ICAM- 1) containing only the two most N terminal of its five immunoglobulin SF domains bind to rhinovirus 3 with the same affinity and kinetics as a fragment with the entire extracellular domain. The fully active two-domain fragments contain 5 or 14 more residues than a previously described fragment that is only partially active. Comparison of X-ray crystal structures show differences at the bottom of domain 2. Four different glycoforms of ICAM- 1 bind with identical kinetics.

scholarly journals Quercetin inhibits inducible ICAM-1 expression in human endothelial cells through the JNK pathway

1999 ◽  
Vol 277 (3) ◽  
pp. C403-C411 ◽  
Author(s):  
Hirotsugu Kobuchi ◽  
Sashwati Roy ◽  
Chandan K. Sen ◽  
Hao G. Nguyen ◽  
Lester Packer
Keyword(s):  
Adhesion Molecule ◽  
Inflammatory Responses ◽  
Surface Expression ◽  
Nuclear Factor Κb ◽  
Intercellular Adhesion Molecule ◽  
Mrna Levels ◽  
Intercellular Adhesion Molecule 1 ◽  
Jnk Pathway ◽  
Tnf Α ◽  
Dose Dependent

The cell adhesion molecule intercellular adhesion molecule-1 (ICAM-1) plays a pivotal role in inflammatory responses. Quercetin (3,3′,4′,5,7-pentahydroxyflavone), a naturally occurring dietary flavonol, has potent anti-inflammatory properties. The effect of quercetin on ICAM-1 expression induced by agonists phorbol 12-myristate 13-acetate (PMA) and tumor necrosis factor-α (TNF-α) in human endothelial cell line ECV304 (ECV) was investigated. Quercetin treatment downregulated both PMA- and TNF-α-induced surface expression, as well as the ICAM-1 mRNA levels, in ECV cells in a dose-dependent (10–50 μM) manner. Quercetin had no effect on PMA- or TNF-α-induced nuclear factor-κB (NF-κB) activation. However, under similar conditions a remarkable dose-dependent downregulation of activator protein-1 (AP-1) activation was observed. This decrease in AP-1 activation was observed to be associated with the inhibitory effects of quercetin on the c-Jun NH2-terminal kinase (JNK) pathway. These results suggest that quercetin downregulates both PMA- and TNF-α-induced ICAM-1 expression via inhibiting both AP-1 activation and the JNK pathway.

scholarly journals Ischemia-reperfusion induced microvascular responses in LDL-receptor −/− mice

1999 ◽  
Vol 276 (5) ◽  
pp. H1647-H1654 ◽  
Author(s):  
Naoharu Mori ◽  
Yoshinori Horie ◽  
Mary E. Gerritsen ◽  
D. Neil Granger
Keyword(s):  
Adhesion Molecule ◽  
Inflammatory Responses ◽  
Ischemia Reperfusion ◽  
Normal Diet ◽  
Intercellular Adhesion Molecule ◽  
High Cholesterol Diet ◽  
Wild Type ◽  
Intercellular Adhesion Molecule 1 ◽  
Rolling Velocity ◽  
Albumin Leakage

The objective of this study was to determine whether the microvascular responses to ischemia and reperfusion (I/R) are altered in an animal model of atherosclerosis, the low-density lipoprotein-receptor knockout (LDLr −/−) mouse. Intravital video microscopy was used to monitor venular wall shear rate, leukocytes rolling velocity, the number of rolling, adherent and emigrated leukocytes, and albumin leakage in cremasteric postcapillary venules of wild-type (B6129) and LDLr −/− mice exposed to 60 min of ischemia and 60 min of reperfusion. The postcapillary venules of LDLr −/− mice exhibited two- to threefold larger increments in the number of adherent leukocytes and a more profound albumin leakage response to I/R than venules in wild-type mice. The exaggerated inflammatory responses noted in LDLr −/− mice placed on a normal diet were not exacerbated by a high-cholesterol diet. Treatment of LDLr −/− mice with either a platelet-activating factor (PAF) receptor antagonist (WEB-2086) or a monoclonal antibody (YN-1) against the endothelial cell adhesion molecule, intercellular adhesion molecule 1 (ICAM-1), markedly attenuated the I/R-induced leukocyte adherence and albumin leakage. These findings indicate that atherogenic mice are more vulnerable to the deleterious microvascular effects of I/R and that PAF-mediated, ICAM-1-dependent leukocyte adhesion contributes to this exaggerated response to I/R.

Hydrodynamic Shear Shows Distinct Roles for LFA-1 and Mac-1 in Neutrophil Adhesion to Intercellular Adhesion Molecule-1

Blood ◽  
1998 ◽  
Vol 92 (5) ◽  
pp. 1626-1638 ◽  
Author(s):  
Sriram Neelamegham ◽  
Andrew D. Taylor ◽  
Alan R. Burns ◽  
C. Wayne Smith ◽  
Scott I. Simon
Keyword(s):  
Shear Stress ◽  
Adhesion Molecule ◽  
Critical Shear Stress ◽  
Intercellular Adhesion Molecule ◽  
Neutrophil Adhesion ◽  
Contact Duration ◽  
Intercellular Adhesion Molecule 1 ◽  
Β2 Integrin ◽  
Adhesion Efficiency ◽  
Kinetics Of

The binding of neutrophil β2 integrin to intercellular adhesion molecule-1 (ICAM-1) expressed on the inflamed endothelium is critical for neutrophil arrest at sites of tissue inflammation. To quantify the strength and kinetics of this interaction, we measured the adhesion between chemotactically stimulated neutrophils and ICAM-1–transfected mouse cells (E3-ICAM) in suspension in a cone-plate viscometer at shear rates typical of venular blood flow (100 s−1 to 500 s−1). The kinetics of aggregation were fit with a mathematical model based on two-body collision theory. This enabled estimation of adhesion efficiency, defined as the probability with which collisions between cells resulted in firm adhesion. The efficiency of β2-integrin–dependent adhesion was highest (∼0.2) at 100 s−1 and it decreased to approximately zero at 400 s−1. Both LFA-1 and Mac-1 contributed equally to adhesion efficiency over the initial 30 seconds of stimulation, but adhesion was entirely Mac-1–dependent by 120 seconds. Two hydrodynamic parameters were observed to influence integrin-dependent adhesion efficiency: the level of shear stress and the intercellular contact duration. Below a critical shear stress (<2 dyn/cm2), contact duration predominantly limited adhesion efficiency. The estimated minimum contact duration for β2-integrin binding was approximately 6.5 ms. Above the critical shear stress (>2 dyn/cm2), the efficiency of neutrophil adhesion to E3-ICAM was limited by both the contact duration and the tensile stress. We conclude that at low shear, neutrophil adhesion is modulated independently through either LFA-1 or Mac-1, which initially contribute with equal efficiency, but differ over the duration of chemotactic stimulation. © 1998 by The American Society of Hematology.

Temperature Dependence of the Photoinduced Degradation and Annealing in a-Si:H

2000 ◽  
Vol 609 ◽  
Author(s):  
Niko Schultz ◽  
P. Craig Taylor
Keyword(s):  
Temperature Dependence ◽  
Room Temperature ◽  
Dangling Bond ◽  
Defect States ◽  
Slow Increase ◽  
Spin Resonance ◽  
The Difference ◽  
Kinetics Of ◽  
Defect Densities ◽  
Spin Densities

ABSTRACTWe investigated the temperature dependence of the production and annealing kinetics of the light induced defect states in a:Si:H by electron spin resonance (ESR). At low temperatures (T ∼ 25 K) the silicon dangling bond production is about half as efficient as it is at 300 K. Defects, which are created below about 100 K, almost entirely anneal at room temperature. A sample of a-Si:H, which is subjected to several photo-excitation and annealing cycles, shows a very slow increase of both the degraded and annealed defect densities. The difference in the spin densities between the annealed and degraded states decreases with an increasing number of degradation/annealing cycles.

scholarly journals Differential Binding of Clonal Variants of Plasmodium falciparum to Allelic Forms of Intracellular Adhesion Molecule 1 Determined by Flow Adhesion Assay

2000 ◽  
Vol 68 (1) ◽  
pp. 264-269 ◽  
Author(s):  
S. Adams ◽  
G. D. H. Turner ◽  
G. B. Nash ◽  
K. Micklem ◽  
C. I. Newbold ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Adhesion Molecule ◽  
Intercellular Adhesion Molecule ◽  
Adhesion Assay ◽  
Intercellular Adhesion Molecule 1 ◽  
Cerebral Disease ◽  
Rolling Velocity ◽  
Frequency Coding ◽  
Intracellular Adhesion Molecule ◽  
Natural Variant

ABSTRACT Adhesion of Plasmodium falciparum-infected erythrocytes to the endothelial ligand intercellular adhesion molecule 1 (ICAM-1) has been implicated in the pathogenesis of cerebral malaria. Recently, a high-frequency coding polymorphism in the N-terminal domain of ICAM-1 (ICAM-1Kilifi) that is associated with susceptibility to cerebral disease in Kenya has been described. Preliminary static adhesion assays suggested that two different selected P. falciparum lines, ITO4-A4 (A4) and ItG-ICAM (ItG), have different properties of binding to the natural variant proteins ICAM-1 and ICAM-1Kilifi. Using a flow adhesion assay system, we have confirmed differences between the two lines in binding of parasitized erythrocytes to the variant ICAM-1 proteins. Total adhesion of ItG-infected erythrocytes to ICAM-1 and ICAM-1Kilifi is greater than that of A4-infected erythrocytes, and erythrocytes infected by both parasite strains show reduced binding to ICAM-1Kilifi. However, under these physiologically relevant flow conditions, we have shown differences between A4 and ItG strains in dynamic rolling behavior on ICAM-1Kilifi. The percentage of erythrocytes infected with A4 that roll on both ICAM-1 and ICAM-1Kilifi is greater than that of those infected with ItG. Also, the rolling velocity of A4-infected erythrocytes on ICAM-1Kilifi is markedly increased compared to that on ICAM-1, in contrast to the rolling velocity of ItG-infected erythrocytes, which is similar on both proteins. These findings suggest that different parasite lines can vary in their avidity for the same host ligand, which may have important consequences for the pathophysiology of P. falciparum malaria.

scholarly journals Cryptococcal Glucuronoxylomannan Inhibits Adhesion of Neutrophils to Stimulated Endothelium In Vitro by Affecting Both Neutrophils and Endothelial Cells

2002 ◽  
Vol 70 (9) ◽  
pp. 4762-4771 ◽  
Author(s):  
Pauline M. Ellerbroek ◽  
Andy I. M. Hoepelman ◽  
Floor Wolbers ◽  
Jaap Jan Zwaginga ◽  
Frank E. J. Coenjaerts
Keyword(s):  
Capsular Polysaccharide ◽  
Inhibitory Effect ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Blocking Antibodies ◽  
Selectin Binding

ABSTRACT Cryptococcal infections are often characterized by a paucity of leukocytes in the infected tissues. Previous research has shown that the capsular polysaccharide glucuronoxylomannan (GXM) inhibits leukocyte migration. In this study we investigated whether the capsular polysaccharide GXM affects the migration of neutrophils (polymorphonuclear leukocytes [PMN]) through the endothelium by interfering with adhesion in a static adhesion model. Pretreatment of PMN with GXM inhibited PMN adhesion to tumor necrosis factor alpha (TNF-α)-stimulated endothelium up to 44%. Treatment of TNF-α-stimulated endothelium with GXM led to a 27% decrease in PMN adhesion. GXM treatment of both PMN and endothelium did not have an additive inhibitory effect. We demonstrated that GXM-induced L-selectin shedding does not play an important role in the detected inhibition of adhesion. L-selectin was still present on PMN in sufficient amounts after GXM treatment, since it could be further inhibited by blocking antibodies. Furthermore, blocking of GXM-related L-selectin shedding did not abolish the GXM-related inhibition of adhesion. GXM most likely exerts its effect on PMN by interfering with E-selectin-mediated binding. The use of blocking monoclonal antibodies against E-selectin, which was shown to decrease adhesion in the absence of GXM, did not cause additive inhibition of PMN adhesion after GXM pretreatment. The use of blocking antibodies also demonstrated that the inhibiting effect found after GXM treatment of endothelium probably involves interference with both intercellular adhesion molecule-1 and E-selectin binding.

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