The adhesion molecules of inflammation

Cronstein, Bruce N.; Weissmann, Gerald

doi:10.1002/art.1780360204

Cited by 246 publications

(104 citation statements)

References 80 publications

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“…For example, our isolation procedure was completed within 24 h, whereas in the other studies it took 48 h, during which time further maturation of DC may have occurred. Activation of endothelial cells with TNF-a also induces the expression of VCAM-1, which is a ligand for CD49d [18].…”

Section: Discussionmentioning

confidence: 99%

Human blood dendritic cells: binding to vascular endothelium and expression of adhesion molecules

Brown

Bedford

Macey

et al. 1997

Clinical and Experimental Immunology

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SUMMARYTo investigate the binding properties of dendritic cells (DC) to vascular endothelium, a comparative analysis was undertaken of DC, monocytes and lymphocytes isolated from the blood of 25 healthy subjects using monolayers of human umbilical vein endothelial cells as the adherence substrate. More blood DC (mean 24% adherence) were adherent to endothelial monolayers than monocytes (mean 18%; P < 0 . 001) and lymphocytes (mean 12%; P < 0 . 001). When the monolayers were pretreated with tumour necrosis factor-alpha (TNF-a) all leucocyte populations exhibited an increased attachment, but there was still greater binding of DC (mean 37% adherence) in comparison with monocytes (mean 23%; P < 0 . 001) and lymphocytes (mean 18%; P < 0 . 001). Flow cytometric analysis revealed that in relation to monocytes and lymphocytes the DC had a higher surface expression of the adhesion molecules CD11a (P < 0 . 05), CD11c (P < 0 . 005) and CD54 (P < 0 . 005) but a lower prevalence of cells bearing CD49d (mean 38%; P < 0 . 05) and the homing receptor CD62L (mean 14%; P < 0 . 001). CD1a was present on 22% of DC and virtually absent from the surface of monocytes and lymphocytes. The intensity of expression of the b 1 -integrins, CD49c, CD49d and CD49e was greater on DC than lymphocytes and monocytes (P < 0 . 05). Antibody blocking studies demonstrated that DC binding to untreated and TNF-a-treated endothelium was dependent upon the expression of CD11a, CD18 and CD49d, and the simultaneous application of anti-CD18 and anti-CD49d antibodies produced an approximate 70% inhibition of adhesion (P < 0 . 001). Thus, the expression of both b 1 -and b 2 -integrins contributes to the adhesive interaction between DC and endothelium.

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Section: Discussionmentioning

confidence: 99%

Human blood dendritic cells: binding to vascular endothelium and expression of adhesion molecules

Brown

Bedford

Macey

et al. 1997

Clinical and Experimental Immunology

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“…Like other glucocorticoids, Dex induces the synthesis of lipocortin that inhibits the enzyme phospholipase A 2 , thereby preventing the generation of prostaglandins, leukotrienes and PAF which can contribute to the recruitment of leukocytes to the inflammatory site (15,16). In addition, glucocorticoids inhibit the synthesis and activity of cytokines with chemotactic properties, including IL-1 (17,18) and TNF-α (19,20), and their ability to induce the expression of adhesion molecules such as E-selectin, ICAM-1 (21) and VCAM-1 (22).…”

Section: A B D C E Fmentioning

confidence: 99%

Histopathological analysis of rat mesentery as a method for evaluating neutrophil migration: differential effects of dexamethasone and pertussis toxin

Brito

Falcão²,

Saraiva

et al. 1998

Braz J Med Biol Res

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In the present study, histopathological analysis of rat mesentery was used to quantify the effect of two anti-inflammatory agents, dexamethasone (Dex) and pertussis toxin (Ptx), on leukocyte migration. The intravenous injection of Dex (1 mg/kg) and Ptx (1,200 ng) 1 h prior to the intraperitoneal injection of the inflammatory stimuli lipopolysaccharide (LPS) or formyl-methionyl-leucyl-phenylalanine (fMLP) significantly reduced the neutrophil diapedesis (LPS: Ptx = 0.86 ± 0.19 and Dex = 0.35 ± 0.13 vs saline (S) = 2.85 ± 0.59; fMLP: Ptx = 0.43 ± 0.09 and Dex 0.01 ± 0.01 vs S = 1.08 ± 0.15 neutrophil diapedesis/ field) and infiltration (LPS: Ptx = 6.29 ± 1.4 and Dex = 3.06 ± 0.76 vs S = 15.94 ± 3.97; fMLP: Ptx = 3.85 ± 0.56 and Dex = 0.40 ± 0.16 vs S = 7.15 ± 1.17 neutrophils/field) induced by the two agonists in the rat mesentery. The inhibitory effect of Dex and Ptx was clearly visible in the fields nearest the venule (up to 200 µm), demonstrating that these anti-inflammatory agents act preferentially in the transmigration of neutrophils from the vascular lumen into the interstitial space, but not in cell movement in response to a haptotactic gradient. The mesentery of rats pretreated with Dex showed a decreased number of neutrophils within the venules (LPS: Dex = 1.50 ± 0.38 vs S = 4.20 ± 1.01; fMLP: Dex = 0.25 ± 0.11 vs S = 2.20 ± 0.34 neutrophils in the lumen/field), suggesting that this inhibitor may be acting at a step that precedes neutrophil arrival in the inflamed tissue. In contrast to that observed with Dex treatment, the number of neutrophils found in mesenteric venules was significantly elevated in animals pretreated with Ptx (LPS: Ptx = 9.85 ± 2.25 vs S = 4.20 ± 1.01; fMLP: Ptx = 4.66 ± 1.24 vs S = 2.20 ± 0.34 neutrophils in the lumen/field). This discrepancy shows that Ptx and Dex act via different mechanisms and suggests that Ptx prevents locomotion of neutrophils from the vascular lumen to the interstitial space. In conclusion, the method described here is useful for quantifying the inflammatory and anti-inflammatory effect of different substances. The advantage of this histopathological approach is that it provides additional information about the steps involved in leucocyte migration.

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“…Increased expression of VCAM-1 (II), E-selectin (6), CD31 (PECAM-1), and /63 integrin subunit (vitronectin receptor) (12) is present on the endothelial cells of rheumatoid synovium compared with normal or osteoarthritic synovium. A number of antiinflammatory drugs have been shown to affect adhesion molecules and/or leukocyte-endothelial interactions (for review see reference 13). Notably, the expression of ICAM-1 on endothelial cells is reduced by colchicine (14) and dexamethasone (15).…”

Section: Introductionmentioning

confidence: 99%

Effect of gold sodium thiomalate and its thiomalate component on the in vitro expression of endothelial cell adhesion molecules.

Newman¹,

To²,

Robinson³

et al. 1994

J. Clin. Invest.

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Endothelial adhesion molecules play an important role in the tissue recruitment of leukocytes in inflammatory conditions such as rheumatoid arthritis. We have investigated the effect of the antirheumatic drug gold sodium thiomalate on adhesion molecule protein and mRNA expression in cultured human endothelial cells. Gold sodium thiomalate inhibited cytokine (TNF, IL-1, IL-4)-stimulated expression of vascular cell adhesion molecule-i and E-selectin but not intercellular adhesion molecule-i on endothelial cells. Gold sodium thiomalate also suppressed TNF-stimulated increases in vascular cell adhesion molecule-i and E-selectin mRNA levels but had no effect on intercellular adhesion molecule-i mRNA. Thiomalate (mercaptosuccinate), but not gold thioglucose or D-penicillamine, mimics the effect of gold sodium thiomalate at equimolar concentrations. We propose that the inhibition of vascular cell adhesion molecule-i and E-selectin expression by gold sodium thiomalate is due to its thiomalate and not its gold component. Gold sodium thiomalate has a direct effect on endothelial adhesion molecule expression, and this may contribute to its antiinflammatory activity. (J.

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The adhesion molecules of inflammation

Cited by 246 publications

References 80 publications

Human blood dendritic cells: binding to vascular endothelium and expression of adhesion molecules

Human blood dendritic cells: binding to vascular endothelium and expression of adhesion molecules

Histopathological analysis of rat mesentery as a method for evaluating neutrophil migration: differential effects of dexamethasone and pertussis toxin

Effect of gold sodium thiomalate and its thiomalate component on the in vitro expression of endothelial cell adhesion molecules.

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