摘要
Sepsis is a host’s response to an intravascular infection;however, in most patients the disease recurs after a seemingly effective treatment. The reappearance of bacteria in the systemic circulation has been attributed to their ability to enter and hide within host endothelial cells. This study shows that internalized S. aureus is released into circulation by a possible mechanism of exocytosis through actin polymerization. Bacterial cell wall components (permeation enhancers) were significantly more effective in altering endothelial cell monolayer integrity than controls. Vancomycin has been determined to be effective in the treatment of S. aureus infections;however, the microencapsulated formulation of vancomycin was significantly more effective in reducing plasma and intra-tissue S. aureus than the conventional solution formulation. Microencapsulation of vancomycin, using albumin as a matrix, did not alter the bioactivity of the drug.
Sepsis is a host’s response to an intravascular infection;however, in most patients the disease recurs after a seemingly effective treatment. The reappearance of bacteria in the systemic circulation has been attributed to their ability to enter and hide within host endothelial cells. This study shows that internalized S. aureus is released into circulation by a possible mechanism of exocytosis through actin polymerization. Bacterial cell wall components (permeation enhancers) were significantly more effective in altering endothelial cell monolayer integrity than controls. Vancomycin has been determined to be effective in the treatment of S. aureus infections;however, the microencapsulated formulation of vancomycin was significantly more effective in reducing plasma and intra-tissue S. aureus than the conventional solution formulation. Microencapsulation of vancomycin, using albumin as a matrix, did not alter the bioactivity of the drug.
