Prevention of Activated Neutrophil Adhesion to Endothelium by Soluble Adhesion Protein GMP140

Gamble, Jennifer R.; Skinner, Michael P.; Berndt, Michael C.; Vadas, Mathew A.

doi:10.1126/science.1696029

Cited by 234 publications

(117 citation statements)

References 35 publications

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“…1 sP-selectin was shown to prevent activated neutrophil adhesion to EC in vitro. 18 In the present report, no differences were observed in sP-selectin levels between normal controls and asthmatic patients. L-selectin is constitutively expressed on most leucocytes but with varying density.…”

Section: Discussionmentioning

confidence: 46%

Elevation of serum soluble E‐selectin and VCAM‐1 in severe asthma

Hamzaoui

Ammar

et al. 2001

Mediators of Inflammation

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Objective: To investigate the significance of circulating adhesion molecules associated with leucocyteendothelial cell interactions in asthma, serum levels of soluble E (sE)-selectin, soluble P (sP)-selectin, soluble L (sL)-selectin, and soluble vascular cell adhesion molecule-1 (sVCAM-1) were measured in mild, moderate and severe asthma. Method: Serum levels of sE-selectin, sP-selectin, sLselectin, and sVCAM-1 were measured in 32 women with asthma and 30 healthy donors using an enzymelinked immunosorbent assay method. Twenty patients were suffering from severe asthma, and 12 from mild/moderate asthma. Results: Serum sE-selectin and sVCAM-1 levels from patients with asthma were significantly higher than those observed in healthy donors (p < 0.01). The levels of sP-selectin were the same as those of controls. The level of sE-selectin exhibited an important increase in the severe asthmatic patients compared with mild/moderate asthma (p < 0.01). The sVCAM-1 level was increased in severe asthma when compared with healthy controls. There was no correlation between the levels of soluble selectins and the age of the patients. A significant correlation was found between sE-selectin and sVCAM-1 levels. Conclusion: These data indicate that circulating soluble forms of the selectins may have different kinetics during the clinical course of asthma, suggesting that they may reflect different inflammatory pathways in severe asthma. Both sVCAM-1 and sE-selectin may be useful immunological markers for monitoring disease activity in asthma.Key words: Asthma, Inflammation, Selectins IntroductionAdherence of leucocytes to endothelial cells (EC) is a primordial event in the sequence of inflammatory response. Specific cell adhesion molecules, expressed on the surface of leucocytes and/or EC, have been identified. As an initial event during inflammation, leucocytes in the blood stream roll along EC with loose contact, mediated by E-selectin, P-selectin and L-selectin. 1 In the inflammation phase, activation of leucocyte integrins occurs with expression of immunoglobulin-like adhesion proteins on EC, including intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 (VCAM-1). The leucocytes that are tightly bound to EC then migrate into the subendothelial tissue. Soluble forms of these adhesion molecules are released in circulation. Serum levels may be increased in several inflammatory diseases, and particularly in asthma. These circulating forms may be biologically active. 2 Asthma is known as a bronchial chronic inflammatory disorder. 3 Immunological abnormalities during asthma are characterized by marked activation of the immune system, leading to increased cytokine production by activated effector cells and the induction of antigen expression on EC. 4 The factors modulating the activation and recruitment of circulating inflammatory cells to the lung remain partially unknown, but an early step in this process is the interaction of adhesion molecules on circulating cells with those on EC. 5 Severe asthma is supposed t...

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Section: Discussionmentioning

confidence: 46%

Elevation of serum soluble E‐selectin and VCAM‐1 in severe asthma

Hamzaoui

Ammar

et al. 2001

Mediators of Inflammation

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“…The presence of P-selectin on an activated endothelial cell layer plays an essential role in the initiation of a tentative adhesive interaction between the circulating inflammatory cell and activated endothelial cell monolayer [21]. Subsequently, the enhanced expression of endothelial cell-associated PAF has been shown to cause transient adherence of neutrophils to the endothelial cells [22][23][24].…”

Section: Resultsmentioning

confidence: 99%

Protease activation of calcium-independent phospholipase A2 leads to neutrophil recruitment to coronary artery endothelial cells

White¹,

McHowat²

2007

Thrombosis Research

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Introduction-Thrombin or tryptase cleavage of protease-activated receptors (PAR) on human coronary artery endothelial cells (HCAEC) results in activation of a membrane-associated, calciumindependent phospholipase A 2 (iPLA 2 ) that selectively hydrolyzes plasmalogen phospholipids. Atherosclerotic plaque rupture results in a coronary ischemic event in which HCAEC in the ischemic area would be exposed to increased thrombin concentrations in addition to tryptase released by activated mast cells present in the plaque.

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“…1 By contrast, intact platelets may inhibit neutrophil O 2 Ϫ generation and cytotoxicity, whereas leukocyte chemotaxis, adhesion, and O 2 Ϫ generation may be inhibited by plateletreleased NO 5 and soluble P-selectin. 6 Thus, platelets and platelet-released products may influence leukocyte function in a complex manner.…”

mentioning

confidence: 99%

Platelet-Leukocyte Cross Talk in Whole Blood

Lindqvist

et al. 2000

ATVB

190

145

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Abstract-Thrombosis and inflammation involve complex platelet-leukocyte interaction, the details of which are not fully elucidated. Therefore, we investigated cross talk between platelets and leukocytes in whole blood, under the following physiological conditions: at 37°C, with normal calcium concentrations, and with shear force. Platelet P-selectin and leukocyte CD11b expression were used to monitor platelet and leukocyte activation, respectively, and platelet-leukocyte aggregation (PLA) was analyzed. The leukocyte-specific agonist N-formyl-methionyl-leucyl-phenylalanine (10 Ϫ6 mol/L) increased P-selectin-positive platelets from 2.5Ϯ0.1% to 5.1Ϯ0.6% (PϽ0.05). The increase was inhibited by either the platelet-activating factor (PAF) antagonist SR27417, the superoxide anion scavenger superoxide dismutase, the 5-lipoxygenase inhibitor Zileuton, or the 5-lipoxygenase-activating protein inhibitor MK-886, suggesting the involvement of PAF, superoxide anion, and 5-lipoxygenase products in leukocyte-induced platelet activation. The platelet-specific agonist collagen (1 g/mL) increased leukocyte CD11b expression from 2.

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Prevention of Activated Neutrophil Adhesion to Endothelium by Soluble Adhesion Protein GMP140

Cited by 234 publications

References 35 publications

Elevation of serum soluble E‐selectin and VCAM‐1 in severe asthma

Elevation of serum soluble E‐selectin and VCAM‐1 in severe asthma

Protease activation of calcium-independent phospholipase A2 leads to neutrophil recruitment to coronary artery endothelial cells

Platelet-Leukocyte Cross Talk in Whole Blood

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