Interleukin-1 alpha and -beta augment pulmonary artery transendothelial albumin flux in vitro
| Autor: | W. N. Campbell, S. E. Goldblum, X. Ding |
|---|---|
| Rok vydání: | 1992 |
| Předmět: |
Pulmonary and Respiratory Medicine
Time Factors Endothelium Physiology Cell Survival Alpha (ethology) Biology Pulmonary Artery Capillary Permeability chemistry.chemical_compound Physiology (medical) medicine Animals Humans Bovine serum albumin Beta (finance) Cells Cultured Serum Albumin Dose-Response Relationship Drug Tumor Necrosis Factor-alpha Albumin Cell Biology Molecular biology Recombinant Proteins Culture Media Endothelial stem cell medicine.anatomical_structure chemistry Immunology biology.protein Tumor necrosis factor alpha Endothelium Vascular Growth inhibition Cell Division Interleukin-1 |
| Zdroj: | The American journal of physiology. 263(1 Pt 1) |
| ISSN: | 0002-9513 |
| Popis: | Human recombinant interleukin-1 alpha (rIL-1 alpha) and -beta were studied to determine whether either could alter the permeability of bovine pulmonary artery endothelial cell monolayers. Endothelial cells were grown to confluence on filters mounted in chemotaxis chambers placed in wells. Barrier function of the monolayers was assessed by placing 14C-labeled bovine serum albumin ([14C]BSA) in the upper chamber and sampling the lower well for [14C]BSA. rIL-1 alpha induced a significant (P less than 0.01) dose- and time-dependent increase in transendothelial [14C]BSA flux. rIL-1 alpha exposures as brief as 30 min increased permeability, but the increased albumin transfer could not be demonstrated before 4 h after exposure. Exposures up to 6 h were reversible at 24 h. rIL-1 alpha induced significantly (P less than 0.01) greater increments in [14C]BSA flux than did equivalent exposures to rIL-1 beta. No important differences between bovine and human rIL-1 beta were demonstrated. Increased transendothelial flux could not be ascribed to either endothelial cytotoxicity or growth inhibition. There was no additive or synergistic relationship between rIL-1 alpha and human recombinant tumor necrosis factor-alpha. Our studies suggest that IL-1 alpha and -beta may play a role in the pathogenesis of pulmonary vascular leak. |
| Databáze: | OpenAIRE |
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