Increased surface expression of CD11b/CD18 (Mac-1) is not required for stimulated neutrophil adherence to cultured endothelium.

Vedder, Nicholas B.; Harlan, John M.

doi:10.1172/jci113372

Cited by 315 publications

(141 citation statements)

References 43 publications

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“…Quantitative changes in expression have also been associated with increased adherence in vitro [25]. Because several CDl I/CDl 8-mediated functions occur without an increase in their expression on the cell surface [ 17] it is believed that conformational changes are equally if not more important than quantitative changes [13]. Recently it has been suggested that rolling of neutrophils on vascular endothelial cells (an early event in inflammation) mediated by selectins precedes adhesion strengthening through CD11/CD18.…”

Section: Discussionmentioning

confidence: 99%

“…The role of LeuCAMs in adhesive processes is moderated by both quantitative and qualitative changes in their expression [13,16,17]. Monocytes and granulocytes possess internal latent pools of CD lib/CD 18 and CDllc/CD18 which are mobilized to the plasma membrane in response to stimulation by mediators such as the complement fragment C5a, tumour necrosis factor-alpha (TNF-a) and phorbol esters [18].…”

Section: Introductionmentioning

confidence: 99%

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Increased CD11/CD18 expression on peripheral blood leucocytes of patients with sarcoidosis

Shakoor

Hamblin

1992

Clinical and Experimental Immunology

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SUMMARYSarcoidosis is a tnultisystem disease of unknown etiology characterized by non-caseating granulomata, formed mainly from macrophages surrounded by lymphocytes and plasma cells. Using a novel method for the preparation of blood leucocytes for flow cytometry, we report increased expression of LeuCAMs (CD 11/CD 18) on peripheral blood leucocytes of 11 Caucasian and 10 Afro-Caribbean patients with sarcoidosis compared with age-, sex-and race-matched controls. Whilst the percentages ofthe cells expressing CDl 1/CD 18 were no different, the density, expressed as mean fluorescence intensity (MFI), was greater for all leucocytes in sarcoids than in normal individuals. The expression of intercellular adhesion molecule-1 (ICAM-1), a ligand for LFA-1 which is expressed on all leucocytes, was not significantly different from normal, whereas HLA-DR was expressed more intensely on sarcoid monocytes (/" < 001) and blood lymphocytes (P < 0 005) than control cells. Our findings are consistent with leucocyte activation although we were unable to confirm reports of elevated tumour necrosis factor-alpha (TNF-a) in the patients' plasma using an ELISA. Increased expression of adhesion molecules on peripheral blood leucocytes may play a role in the cellular extravasation, aggregation, and granuloma formation seen in sarcoidosis.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Increased CD11/CD18 expression on peripheral blood leucocytes of patients with sarcoidosis

Shakoor

Hamblin

1992

Clinical and Experimental Immunology

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“…Treatment of these patients with the 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors lovastatin or simvastatin for 6 weeks decreases total and LDL cholesterol plasma levels, as well as monocyte CD11b surface expression, and results in a substantial reduction of monocyte adhesion to endothelium (74). The regulation of CD11b surface expression is dissociated from adhesive function, which requires its activation (75,76). Thus, the pronounced decrease in adhesion after treatment with statins appears to be independent of the slight reduction in CD11b expression.…”

Section: Statins Inhibit Monocyte Adhesiveness In Patients With Hypermentioning

confidence: 99%

Effects of Oxidized Low Density Lipoprotein, Lipid Mediators and Statins on Vascular Cell Interactions

Weber¹,

Erl²,

Weber³

et al. 1999

CCLM

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The integrin heterodimer CD11b/CD18 (␣M␤2, Mac-1, CR3) expressed on monocytes or polymorphonuclear leukocytes (PMN) is a receptor for iC3b, fibrinogen, heparin, and for intercellular adhesion molecule (ICAM)-1 on endothelium, crucially contributing to vascular cell interactions in inflammation and atherosclerosis. In this report, we summarize our findings on the effects of lipid mediators and lipid-lowering drugs. Exposure of endothelial cells to oxidized low density lipoprotein (oxLDL) induces upregulation of ICAM-1 and increases adhesion of monocytic cells expressing Mac-1. Inhibition experiments show that monocytes use distinct ligands, i.e. ICAM-1 and heparan sulfate proteoglycans for adhesion to oxLDL-treated endothelium. An albumin-transferable oxLDL activity is inhibited by the antioxidant pyrrolidine dithiocarbamate (PDTC), while 8-epi-prostaglandin F2␣ (8-epi-PGF2␣) or lysophosphatidylcholine had no effect, implicating yet unidentified radicals. Sequential adhesive and signaling events lead to the firm adhesion of rolling PMN on activated and adherent platelets, which may occupy areas of endothelial denudation. Shear-resistant arrest of PMN on thrombin-stimulated platelets in flow conditions requires distinct regions of Mac-1, involving its interactions with fibrinogen bound to platelet ␣IIb␤3, and with other platelet ligands. Both arrest and adhesion strengthening under flow are stimulated by platelet-activating factor and leukotriene B4, but not by the chemokine receptor CXCR2. We tested whether Mac-1-dependent monocyte adhesiveness is affected by inhibitors of hydroxy-methylglutaryl-Coenzyme A reductase (statins) which improve morbidity and survival of patients with coronary heart disease. As compared to controls, adhesion of isolated monocytes to endothelium ex vivo was increased in patients with hypercholesterolemia. Treatment with statins decreased total and low density lipoprotein (LDL) cholesterol plasma levels, surface expression of Mac-1, and resulted in a dramatic reduction of Mac-1-mediated monocyte adhesion to endothelium. The inhibition of monocyte adhesion was reversed by mevalonate but not LDL in vitro, indicating that isoprenoid precursors are crucial for adhesiveness of Mac-1. Such effects may crucially contribute to the clinical benefit of statins, independent of cholesterol-lowering, and may represent a paradigm for novel, anti-inflammatory mechanisms of action by this class of drugs.

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“…It is now clear that although the number of CDI Ib/CD18 molecules is increased on the surface of stimulated neutrophils, the increased expression of these adhesive molecules on the leukocyte surface is neither necessary nor sufficient for the increased CDI 1 bKD18-mediated adhesiveness of stimulated neutrophils either to endothelium or to other neutrophils. In other words, affinity modulation is required (19)(20)(21). Recent studies in which transfected, mutated leukocyte integrin molecules were assessed for their adhesiveness indicate that stimulated adhesiveness depends upon certain critical cytoplasmic domains of CD18 (l6,22).…”

Section: Integrinsmentioning

confidence: 99%

The adhesion molecules of inflammation

Cronstein

Weissmann

1993

Arthritis & Rheumatism

246

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Increased surface expression of CD11b/CD18 (Mac-1) is not required for stimulated neutrophil adherence to cultured endothelium.

Abstract: The mechanism whereby the human neutrophil membrane het-

Cited by 315 publications

References 43 publications

Increased CD11/CD18 expression on peripheral blood leucocytes of patients with sarcoidosis

Increased CD11/CD18 expression on peripheral blood leucocytes of patients with sarcoidosis

Effects of Oxidized Low Density Lipoprotein, Lipid Mediators and Statins on Vascular Cell Interactions

The adhesion molecules of inflammation

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