Role of endothelial-leukocyte adhesion molecule 1 (ELAM-1) in neutrophil-mediated lung injury in rats.

Mulligan, Michael S.; Varani, James; Dame, Michael K.; Lane, Caryl; Smith, C. W.; Anderson, Donald C.; Ward, Peter A.

doi:10.1172/jci115446

Cited by 361 publications

(137 citation statements)

References 27 publications

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“…This is supported by reports of increased E-selectin, but not P-selectin, expression in RA compared with noninflamed synovium (15,16). Also, some in vivo animal models of cytokineinduced inflammation, such as immune complexmediated organ injury and neutrophil-mediated hypoxia-reperfusion injury, have been demonstrated to be primarily dependent on E-selectin expression (12,43). This contrasts with the results reported by Grober et a1 (44), who found that antibodies specific for P-selectin consistently inhibited >90% of monocyte adhesion to frozen sections of RA tissues, whereas antibodies to E-selectin variably blocked only 20-50% of monocyte attachment.…”

Section: Discussionmentioning

confidence: 99%

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Effects of pulse methylprednisolone on cell adhesion molecules in the synovial membrane in rheumatoid arthritis. Reduced E‐selectin and intercellular adhesion molecule 1 expression

Youssef

Triantafillou

Parker

et al. 1996

Arthritis & Rheumatism

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Objective. To investigate the effects of a 1,000-mg intravenous pulse of methylprednisolone succinate (MP) on cell adhesion molecule expression on the synovial vascular endothelium in patients with rheumatoid arthritis (RA).Methods. Sequential arthroscopic biopsy samples were taken before and 24 hours after MP administration (10 patients) and at the time of RA flare (2 patients) and after retreatment with MP (1 patient). Immunoperoxidase staining for E-selectin (CD62E), P-selectin (CD62P), intercellular adhesion molecule 1 (ICAM-1; CD54) and platelet-endothelial cell adhesion molecule (PECAM; CD31) was performed, and the staining was quantified by color video image analysis.Results. MP caused a rapid (within 24 hours) and substantial decrease in the expression of E-selectin on the synovial vascular endothelium, with a smaller reduction in ICAM-1 expression on synovial vascular endothelium and the synovial lining. There were no similar effects on synovial membrane P-selectin or PECAM expression.Conclusion. A potential mechanism by which MP

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Section: Discussionmentioning

confidence: 99%

“…9). However, in vivo models of inflammatory disease display a degree of differential selectin expression, depending on the disease process and the organ involved, which suggests different functional roles for individual selectins (12).…”

mentioning

confidence: 99%

Effects of pulse methylprednisolone on cell adhesion molecules in the synovial membrane in rheumatoid arthritis. Reduced E‐selectin and intercellular adhesion molecule 1 expression

Youssef

Triantafillou

Parker

et al. 1996

Arthritis & Rheumatism

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“…Up-regulation of circulating E-selectin and ICAM-1 is found in the airways of patients with asthma and cystic fibrosis [15,16], where marked airway infiltration by eosinophils or neutrophils occurs. Antibodies against E-selectin and ICAM-1 block neutrophil extravasation in rat lungs [33], and inhibit neutrophil trafficking into the inflamed lungs of a rabbit [34]. VCAM-1 is involved in the recruitment of eosinophils, monocytes/macrophages and lymphocytes into the lungs [19,20].…”

Section: Discussionmentioning

confidence: 99%

Up-regulation of circulating adhesionmolecules in bronchiectasis

Zheng

Tipoe²,

Lam³

et al. 2000

Eur Respir J

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Adhesion molecules are expressed on the surface of endothelial cells and leukocytes and are responsible for mediating the migration of intravascular leukocytes into inflamed tissue. Intensive recruitment of neutrophils into the airways occurs in bronchiectasis, although little is known about the role of adhesion molecules in this process.The authors, therefore, determined serum levels of E-selectin, intercellular adhesion molecule (ICAM)-1 and vascular adhesion molecule (VCAM)-l in stable bronchiectasis patients (n=37) and healthy control subjects (n=17), and evaluated their relationship with clinical markers of disease severity in bronchiectasis.Serum levels of E-selectin, ICAM-1 and VCAM-1 in bronchiectasis patients were significantly higher than those in control subjects (p=0.02, <0.0001 and 0.0002 respectively). Both E-selectin and ICAM-1 levels were inversely related to forced expiratory volume in one second (FEV1)% predicted (r=-0.57, p<0.001; and r=-0.53, p=0.001 respectively), and FVC% predicted (r=-0.52, p=0.002; and r=-0.46, p=0.005). This was not the case for VCAM-1 levels. There was a correlation between serum ICAM-1 levels and 24 h sputum volume (r=0.34, p= 0.04). Serum E-selectin and ICAM-1, but not VCAM-1, levels showed correlation with the number of lung lobes affected by bronchiectasis (r=0.35, p=0.04 and r=0.34, p=0.04 respectively).These original observations strongly suggest that E-selectin, intercellular adhesion molecule-1 and Vascular adhesion molecule-1 could play a significant role in the pathogenesis of bronchiectasis. Eur Respir J 2000; 16: 691±696.

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“…Inhibition of E-selectin [2,3] or P-selectin [3,4] by blocking antibodies compromises the peritoneal emigration of neutrophils during peritonitis induced by intraperitoneal injections of glycogen or thioglycollate. Mutant mice deficient in P-selectin [5][6][7] demonstrate compromised neutrophil emigration in the peritoneal cavity during Streptococcus pneumoniae or thioglycollate-induced peritonitis, but mutants deficient in E-selectin show no such defects [4,7].…”

Section: Introductionmentioning

confidence: 99%

Combinatorial requirements for adhesion molecules in mediating neutrophil emigration during bacterial peritonitis in mice

Mizgerd

Quinlan

LeBlanc

et al. 1998

Journal of Leukocyte Biology

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To investigate the requirements for adhesion molecules in neutrophil emigration during peritonitis, mice received intraperitoneal injections of Streptococcus pneumoniae while the functions of multiple adhesion molecules were blocked. Emigration after 4 h was compromised by antibodies against ICAM-1 or genetic deficiency of ICAM-1. Anti-CD11a/CD18 antibodies decreased emigration in ICAM-1 mutant mice, suggesting that ICAM-1 independent emigration requires CD11/CD18 complexes. In contrast, mice mutant in ICAM-1 plus E-selectin showed no defect in emigration, suggesting that E-selectin commits neutrophils to an ICAM-1-dependent pathway during streptococcal peritonitis. However, in mutant mice lacking the three endothelial adhesion molecules E-selectin, P-selectin, and ICAM-1, emigration after 4 h was significantly compromised. Thus, P-selectin is essential to ICAM-1-and E-selectin-independent acute peritoneal inflammation. After 24 h of peritonitis, there were no differences between WT and E-selectin/P-selectin/ ICAM-1 mutant mice, demonstrating that these endothelial adhesion molecules are not essential to neutrophil emigration during later stages of peritonitis. J. Leukoc. Biol. 64: 291-297; 1998.

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Role of endothelial-leukocyte adhesion molecule 1 (ELAM-1) in neutrophil-mediated lung injury in rats.

Cited by 361 publications

References 27 publications

Effects of pulse methylprednisolone on cell adhesion molecules in the synovial membrane in rheumatoid arthritis. Reduced E‐selectin and intercellular adhesion molecule 1 expression

Effects of pulse methylprednisolone on cell adhesion molecules in the synovial membrane in rheumatoid arthritis. Reduced E‐selectin and intercellular adhesion molecule 1 expression

Up-regulation of circulating adhesionmolecules in bronchiectasis

Combinatorial requirements for adhesion molecules in mediating neutrophil emigration during bacterial peritonitis in mice

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