The extracellular adherence protein from Staphylococcus aureus inhibits neutrophil binding to endothelial cells.
Extracellular adherence protein (Eap) from Staphylococcus aureus inhibits the adherence of neutrophils to nonstimulated and tumor necrosis factor alpha-stimulated endothelial cells in both static adhesion assays and flow adhesion assays. Consequently, Eap also impaired their transendothelial migration. During an S. aureus infection, Eap may thus serve to reduce inflammation by inhibiting neutrophil adhesion and extravasation.
Haggar
Axana
A
Division of Clinical Bacteriology, Department of Laboratory Medicine, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden.
Ehrnfelt
Cecilia
C
Holgersson
Jan
J
Flock
Jan-Ingmar
JI
D001426:Bacterial Proteins / Q000494:pharmacology*; D002448:Cell Adhesion / Q000187:drug effects; D002478:Cells, Cultured; D002634:Chemotaxis, Leukocyte / Q000187:drug effects; D042783:Endothelial Cells / Q000166:cytology* / Q000187:drug effects*; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000276:immunology / Q000378:metabolism; D009504:Neutrophils / Q000166:cytology* / Q000187:drug effects* / Q000382:microbiology; D016601:RNA-Binding Proteins / Q000494:pharmacology*; D013211:Staphylococcus aureus; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology
D001426:Bacterial Proteins; C444739:Eap-N protein, Staphylococcus aureus; D016601:RNA-Binding Proteins; D014409:Tumor Necrosis Factor-alpha; D018799:Intercellular Adhesion Molecule-1