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Infect. Immun., 04 1995, 1380-1386, Vol 63, No. 4
M Soell, M Diab, G Haan-Archipoff, A Beretz, C Herbelin, B Poutrel and JP Klein
In order to examine the possible implication of capsular polysaccharide
(CP) types 5 and 8 (CP5 and CP8) from Staphylococcus aureus in the
pathological mechanism associated with staphylococcal infections, we tested
the immunomodulatory effects of CP5 and CP8 on human epithelial KB cells,
endothelial cells, and monocytes. Using biotinylated CP5 and CP8, we
provide evidence that both CPs bind to KB cells, endothelial cells, and
monocytes in a dose- and calcium-dependent manner through specific
interactions. These results were confirmed by competition experiments using
soluble cell extracts. Furthermore, we show that CPs bind to identical cell
membrane receptors on all three types of human cells and that human normal
serum contains a factor(s) which inhibits the binding of both CPs to human
KB cells, endothelial cells, and monocytes. The ability of CP5 and CP8 to
stimulate the production of cytokines by the human cells was then examined.
CP5 and CP8 trigger KB cells to produce interleukin-8 (IL-8); endothelial
cells to produce IL- 8 and IL-6; and monocytes to produce IL-8, IL-6, IL-1
beta, and tumor necrosis factor alpha. The release of cytokines by all
three types of cells is time dependent and dose dependent, and the tumor
necrosis factor alpha production by monocytes is not affected by the
addition of polymyxin B. We further confirm that human normal serum
inhibits the immunomodulatory effects of both polysaccharides on each kind
of cell. These results confirm that S. aureus CPs act as bacterial adhesins
having immunomodulatory effects for human cells.
Copyright © 1995, American Society for Microbiology
Capsular polysaccharide types 5 and 8 of Staphylococcus aureus bind specifically to human epithelial (KB) cells, endothelial cells, and monocytes and induce release of cytokines
INSERM Unite 392, Faculte de Pharmacie, Illkirch, France.
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