SEB is cytotoxic and alters EC barrier function through protein tyrosine phosphorylation in vitro
| Autor: | X. Ding, M. Jett, M. Fitzpatrick, W. N. Campbell, P. Gemski, S. E. Goldblum |
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| Rok vydání: | 1997 |
| Předmět: |
Pulmonary and Respiratory Medicine
Staphylococcus aureus Cell Membrane Permeability Cell Survival Physiology Lactams Macrocyclic Genistein chemical and pharmacologic phenomena Pulmonary Artery Biology Enterotoxins chemistry.chemical_compound Physiology (medical) Benzoquinones Animals Humans Trypsin Polymyxins Cycloheximide Enzyme Inhibitors Phosphorylation Tyrosine Bovine serum albumin Cells Cultured Barrier function Quinones Temperature Biological Transport Serum Albumin Bovine hemic and immune systems Chemotaxis Tyrosine phosphorylation Cell Biology Protein-Tyrosine Kinases Isoflavones Molecular biology biological factors Endothelial stem cell Kinetics Rifabutin chemistry Herbimycin Immunology biology.protein Cattle Endothelium Vascular |
| Zdroj: | American Journal of Physiology-Lung Cellular and Molecular Physiology. 273:L31-L39 |
| ISSN: | 1522-1504 1040-0605 |
| DOI: | 10.1152/ajplung.1997.273.1.l31 |
| Popis: | We studied whether Staphylococcal enterotoxin B (SEB) has direct effects on endothelial cells (EC) in the absence of effector cells or their products. Bovine or human pulmonary artery EC were grown to confluence on filters mounted in chemotaxis chambers. Barrier function was assessed by placing [14C]bovine serum albumin in the chamber and sampling the lower well for 14C activity. SEB exposures induced a significant (P < 0.001) dose- and time-dependent increase in albumin flux across both bovine and human EC monolayers. Albumin flux was temperature dependent, and cycloheximide pretreatment of the monolayers did not block the SEB-induced increase in permeability. Preincubation of SEB with trypsin or anti-SEB antibody significantly (P < 0.0001) reduced the effect, whereas pretreatment with polymyxin B did not. SEB at > or = 10 micrograms/ml significantly (P < 0.03) increased EC injury as measured by 51Cr release in a dose- and time-dependent manner. Herbimycin and genistein, inhibitors of protein tyrosine kinases, each protected against SEB-induced cytotoxicity, barrier dysfunction, and intercellular gap formation. We conclude that SEB perturbs endothelial barrier function and viability in the absence of effector cells or their mediators. |
| Databáze: | OpenAIRE |
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