Soluble Adhesion Molecules E-Cadherin, Intercellular Adhesion Molecule-1, and E-Selectin as Lung Cancer Biomarkers

CHEST Journal ◽  
2010 ◽  
Vol 138 (5) ◽  
pp. 1173-1179 ◽  
Author(s):  
Athena Gogali ◽  
Konstantinos Charalabopoulos ◽  
Iris Zampira ◽  
Athanasios K. Konstantinidis ◽  
Fanny Tachmazoglou ◽  
...  
Perfusion ◽  
1998 ◽  
Vol 13 (5) ◽  
pp. 322-327 ◽  
Author(s):  
Hilary J Williams ◽  
Naomi Rebuck ◽  
Martin J Elliott ◽  
Adam Finn

A consequence of cardiopulmonary bypass (CPB) in young children is postoperative capillary leak and associated pulmonary dysfunction. Neutrophils sequester in the lungs and may contribute to functional endothelial damage. The endothelial adhesion molecules, E-selectin and intercellular adhesion molecule-1 (ICAM-1), mediate sequential steps in adhesion by binding to leucocyte ligands. Circulating forms of these proteins have been identified. We studied changes in the plasma concentrations of soluble E-selectin and soluble ICAM-1 using fixed phase immunoassays, and associated leucocyte counts in 10 paediatric patients undergoing CPB. Concentrations of soluble L-selectin and soluble ICAM-1 consistently fell during CPB from preoperative levels of 89 ± 17 ng/ml (mean ± 2SEM) and 218 + 61 ng/ml, respectively, to 39 ± 7 ng/ml and 84 ± 24 ng/ml, respectively at the beginning of maximum hypothermia. The haemodilution that occurred during CPB largely explained this fall, but not the more marked decrease in white cell counts that also occurred over this period (6.7 ± 1.1 to 1.7 ± 0.5 × 109/l) which may reflect increased leucocyte sequestration. By 24 h postoperatively, levels of both soluble adhesion molecules approached preoperative concentrations, as did lymphocyte counts. In marked contrast, neutrophil counts rose appreciably towards the end of CPB, and continued to rise to a maximum of 10.9 ± 3.1 ×109/l during the immediate postoperative period and remained at these elevated levels 24 h later. Major consistent changes in circulating leucocyte numbers which occur early in cardiopulmonary bypass may reflect changes in adhesion to the endothelium and consequent sequestration. Alterations in the levels of soluble adhesion proteins may influence these processes.


2003 ◽  
Vol 285 (5) ◽  
pp. L996-L1005 ◽  
Author(s):  
Rainer Kiefmann ◽  
Kai Heckel ◽  
Martina Dörger ◽  
Sonja Schenkat ◽  
Mechthild Stoeckelhuber ◽  
...  

During systemic inflammation, recruitment and activation of leukocytes in the pulmonary microcirculation may result in a potentially life-threatening acute lung injury. We elucidated the role of the poly(ADP-ribose) synthetase (PARS), a nucleotide-polymerizing enzyme, in the regulation of leukocyte recruitment within the lung with regard to the localization in the pulmonary microcirculation and in correlation to hemodynamics in the respective vascular segments and expression of intercellular adhesion molecule 1 during endotoxemia. Inhibition of PARS by 3-aminobenzamide reduced the endotoxin-induced leukocyte recruitment within pulmonary arterioles, capillaries, and venules in rabbits as quantified by in vivo fluorescence microscopy. Microhemodynamics and thus shear rates in all pulmonary microvascular segments remained constant. Simultaneously, inhibition of PARS with 3-aminobenzamide suppressed the endotoxin-induced adhesion molecules expression as demonstrated for intercellular adhesion molecule 1 by immunohistochemistry and Western blot analysis. We confirmed this result with the use of PARS knockout mice. The inhibitory effect of 3-aminobenzamide on leukocyte recruitment was associated with a reduction of pulmonary capillary leakage and edema formation. We first provide evidence that PARS activation mediates the leukocyte sequestration in pulmonary microvessels through upregulation of adhesion molecules. As reactive oxygen species released from leukocyte are supposed to cause an upregulation of adhesion molecules we conclude that PARS inhibition contributes to termination of this vicious cycle and inhibits the inflammatory process.


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