Perflubron attenuates neutrophil adhesion to activated endothelial cells in vitro
| Autor: | Catherine M. Woods, Elisabeth S. Kornbrust, Gerald G. Neslund, Stephen F. Flaim |
|---|---|
| Rok vydání: | 2000 |
| Předmět: |
Pulmonary and Respiratory Medicine
Lipopolysaccharides Pathology medicine.medical_specialty Umbilical Veins Physiology Neutrophils Intercellular Adhesion Molecule-1 Fluorescent Antibody Technique Lung injury In Vitro Techniques Diffusion chemistry.chemical_compound Blood Substitutes Physiology (medical) E-selectin Cell Adhesion Medicine Humans Cells Cultured Fluorocarbons Lung biology business.industry Perflubron Respiratory disease Cell Biology Pneumonia medicine.disease Hydrocarbons Brominated Up-Regulation Endothelial stem cell medicine.anatomical_structure chemistry biology.protein Endothelium Vascular business E-Selectin Infiltration (medical) |
| Zdroj: | American journal of physiology. Lung cellular and molecular physiology. 278(5) |
| ISSN: | 1040-0605 |
| Popis: | Infiltration of activated neutrophils into the lung appears to be a key element in the severe lung injury that develops in animal models of acute lung injury. Partial liquid ventilation with perflubron has been shown to ameliorate tissue damage compared with conventional mechanical ventilation in acute lung injury models. Pilot experiments indicated that indirect exposure to perflubron could modulate the degree to which subsequent neutrophil binding to endothelial cell monolayers was upregulated after lipopolysaccharide activation. Endothelial cell monolayers preexposed to perflubron showed >40% reductions in the surface steady-state levels of E-selectin and intercellular adhesion molecule-1 achieved after proinflammatory activation ( P < 0.05), which correlated with a reduction in the real-time association constants measured by biosensor techniques. These results indicate that direct contact with the perflubron liquid phase is not necessary to attenuate inflammatory responses. Rather, diffusion of perflubron from the alveolar space into the adjacent pulmonary vascular endothelial layer may modulate neutrophil adhesion and thereby reduce the rate of infiltration of activated neutrophils into the injured lung. |
| Databáze: | OpenAIRE |
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