Chemoattractant‐induced firm adhesion of leukocytes to vascular endothelium <i>in vivo</i> is critically dependent on initial leukocyte rolling

Lindbom, Lennart; Xie, Xun; Raud, J.; Hedqvist, Per

doi:10.1111/j.1748-1716.1992.tb09442.x

Cited by 123 publications

(110 citation statements)

References 31 publications

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“…This sulfated homopolymer of fucose did not lower the circulating leukocyte count in this study or the number of freeflowing cells through microvessels in other studies (47,48), making leukocytopenia an unlikely explanation for the very profound reduction in leukocyte rolling. Since fucoidin binds to and avidly inhibits both L-selectin and P-selectin interactions, one possible explanation for the greater effectiveness of fucoidin than antiselectin antibody therapy is another adhesive mechanism inhibitable by the carbohydrate polymer.…”

Section: Discussioncontrasting

confidence: 58%

Therapeutic potential of inhibiting leukocyte rolling in ischemia/reperfusion.

Kubes¹,

Jutila²,

Payne³

1995

J. Clin. Invest.

242

147

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Leukocyte rolling has been postulated to be mandatory for subsequent leukocyte adhesion and tissue injury observed during ischemia/reperfusion. The objective of this study was to systematically assess this hypothesis at the microvascular level by examining the effects of various concentrations of a selectin-binding carbohydrate (fucoidin) on the increased rolling and adhesion of leukocytes in postischemic venules. The contribution of L-selectin and/or P-selectin to leukocyte rolling were also assessed in this model. Using intravital microscopy we observed that 60 min of ischemia followed by reperfusion caused a profound increase in leukocyte rolling and adhesion. A high dose of fucoidin (25 mg/kg) reduced leukocyte rolling by > 90% and significantly reduced leukocyte adhesion, whereas a lower dose of fucoidin still reduced leukocyte rolling by 60% but had no effect on leukocyte adhesion. Moreover, despite the profound reduction in leukocyte rolling with fucoidin, the remaining rolling cells were able to firmly adhere via a CD18-dependent mechanism, particularly in those postcapillary venules with reduced (30-50%) shear rates. The increased rolling was also reduced 60% by either an anti-P-selectin antibody, an anti-L-selectin antibody, or a combination of the two antibodies, but this reduction in rolling cells did not translate into significantly reduced leukocyte adhesion. Our data suggest that L-selectin, P-selectin, and a fucoidin-sensitive pathway contribute to the significant increase in reperfusion-induced leukocyte rolling. However, targeting leukocyte rolling as a form of therapy requires very significant efficacy (> 90%) to achieve reasonable (-50%) attenuation in leukocyte adhesion in postischemic venules. (J. Clin. Invest. 1995Invest. . 95:2510Invest. -2519

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Section: Discussioncontrasting

confidence: 58%

Therapeutic potential of inhibiting leukocyte rolling in ischemia/reperfusion.

Kubes¹,

Jutila²,

Payne³

1995

J. Clin. Invest.

242

147

View full text Add to dashboard Cite

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“…For instance, inhibition of selectin binding to sialyl Lewis X by the polysaccharide fucoidin, results in reduction of PMN rolling and extravasation. 40,41 These sugars may be expressed on several membrane proteins, 42 including those mediating L-selectin and P-selectin binding to their counterligands. 37 It is of interest that a recent study has reported a role for complex sugars in mediating the anti-inflammatory effects of heparin derivatives.…”

Section: Discussionmentioning

confidence: 99%

A Novel Biological Activity for Galectin-1

Cao

Cerchiaro

et al. 2003

The American Journal of Pathology

136

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Galectin-1 (Gal-1), the prototype of a family of ␤-galactoside-binding proteins, has been shown to attenuate experimental acute and chronic inflammation. In view of the fact that endothelial cells (ECs), but not human polymorphonuclear leukocytes (PMNs), expressed Gal-1 we tested here the hypothesis that the protein could modulate leukocyte-EC interaction in inflammatory settings. In vitro, human recombinant (hr) Gal-1 inhibited PMN chemotaxis and trans-endothelial migration. These actions were specific as they were absent if Gal-1 was boiled or blocked by neutralizing antiserum. In vivo, hrGal-1 (optimum effect at 0.3 g equivalent to 20 pmol) inhibited interleukin-1␤-induced PMN recruitment into the mouse peritoneal cavity. Intravital microscopy analysis showed that leukocyte flux, but not their rolling velocity, was decreased by an anti-inflammatory dose of hrGal-1. Binding of biotinylated Gal-1 to resting and postadherent human PMNs occurred at concentrations inhibitory in the chemotaxis and transmigration assays. In addition , the pattern of Gal-1 binding was differentially modulated by PMN or EC activation.

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“…Sheep anti-mouse-glomerular basement membrane (GBM) 3 Ab was prepared as described previously, except that murine cortices were sonicated following homogenization (26). Normal sheep globulin (sheep Ig), prepared from nonimmune sheep serum using the same protocol, served as a control Ab.…”

Section: Antibodiesmentioning

confidence: 99%

“…This interaction allows the leukocytes to respond to activating stimuli and subsequently arrest on the endothelial surface (2). Several studies in which leukocyte rolling has been inhibited or eliminated have demonstrated that the rolling interaction is critical in allowing leukocytes to undergo adhesion (3)(4)(5)(6). Moreover, direct examination of the microvasculature using in vivo microscopy has repeatedly demonstrated that these interactions occur almost exclusively in postcapillary venules, primarily because expression of the endothelial adhesion molecules which mediate leukocyte rolling, particularly P-and E-selectin, is restricted to these sites (7,8).…”

mentioning

confidence: 99%

Leukocyte Recruitment to the Inflamed Glomerulus: A Critical Role for Platelet-Derived P-Selectin in the Absence of Rolling

Kuligowski

Kitching

Hickey

2006

The Journal of Immunology

122

153

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The renal glomerulus is one of the few sites within the microvasculature in which leukocyte recruitment occurs in capillaries. However, due to the difficulty of directly visualizing the glomerulus, the mechanisms of leukocyte recruitment to glomerular capillaries are poorly understood. To overcome this, we rendered murine kidneys hydronephrotic to allow the visualization of the functional glomerular microvasculature during an inflammatory response. These experiments demonstrated that following infusion of anti-glomerular basement membrane (GBM) Ab, leukocytes became adherent in glomerular capillaries via a process of immediate arrest, without undergoing prior detectable rolling. However, despite the absence of rolling, this recruitment involved nonredundant roles for the P-selectin/P-selectin glycoprotein ligand-1 and β2 integrin/ICAM-1 pathways, suggesting that a novel form of the multistep leukocyte adhesion cascade occurs in these vessels. Anti-GBM Ab also increased glomerular P-selectin expression and induced a P-selectin-independent increase in platelet accumulation. Moreover, platelet depletion prevented both the increase in glomerular P-selectin, and the leukocyte recruitment induced by anti-GBM Ab. Furthermore, depletion of neutrophils and platelets also prevented the increase in urinary protein excretion induced by anti-GBM Ab, indicating that their accumulation in glomeruli contributed to the development of renal injury. Finally, infusion of wild-type platelets into P-selectin-deficient mice restored the ability of glomeruli in these mice to support leukocyte adhesion. Together, these data indicate that anti-GBM Ab-induced leukocyte adhesion in glomeruli occurs via a novel pathway involving a nonrolling interaction mediated by platelet-derived P-selectin.

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Chemoattractant‐induced firm adhesion of leukocytes to vascular endothelium in vivo is critically dependent on initial leukocyte rolling

Cited by 123 publications

References 31 publications

Therapeutic potential of inhibiting leukocyte rolling in ischemia/reperfusion.

Therapeutic potential of inhibiting leukocyte rolling in ischemia/reperfusion.

A Novel Biological Activity for Galectin-1

Leukocyte Recruitment to the Inflamed Glomerulus: A Critical Role for Platelet-Derived P-Selectin in the Absence of Rolling

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