Invasion and killing of XXXX endothelial cells by viridans group streptococci.

@entity1 @entity6586 @entity9858 @entity137 @entity3167 @entity9190 @entity10612 @entity6419 @entity885 @entity731 @entity11119 @entity291 @entity20842 @entity884
Colonization of the cardiovascular endothelium by viridans group streptococci can result in @entity884 and possibly @entity731 ; however, the mechanisms of pathogenesis are poorly understood. We investigated the ability of selected oral streptococci to infect monolayers of @entity1 umbilical vein endothelial cells (HUVEC) in 50% @entity1 plasma and to produce @entity137 . Planktonic @entity9190 CH1 killed HUVEC over a 5-h period by peroxidogenesis (alpha-hemolysin) and by acidogenesis but not by production of protein exotoxins. HUVEC were protected fully by addition of supplemental buffers and @entity291 liver catalase to the culture medium. Streptococci were also found to invade HUVEC by an endocytic mechanism that was dependent on polymerization of actin microfilaments and on a functional cytoskeleton, as indicated by inhibition with @entity11119 and @entity10612 . Electron microscopy revealed streptococci attached to HUVEC surfaces via numerous fibrillar structures and bacteria in membrane-encased cytoplasmic vacuoles. Following invasion by @entity9190 CH1, HUVEC monolayers showed 63% cell lysis over 4 h, releasing 64% of the total intracellular bacteria into the culture medium; however, the bacteria did not multiply during this time. The ability to invade HUVEC was exhibited by selected strains of @entity9190 , @entity885 , @entity6586 , @entity6419 , and @entity9858 but only weakly by @entity20842 . Comparison of isogenic pairs of @entity9190 revealed a requirement for several surface proteins for maximum host cell invasion: glucosyltransferase, the @entity3167 -binding protein Hsa, and the hydrophobicity/coaggregation proteins CshA and CshB. Deletion of genes for the antigen I/II adhesins, SspA and SspB, did not affect invasion. We hypothesize that peroxidogenesis and invasion of the cardiovascular endothelium by viridans group streptococci are integral events in the pathogenesis of @entity884 and @entity731 .
