Sandbox 300: Difference between revisions

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Zoé Durrenberger

Revision as of 17:26, 16 December 2011 view source ZoÃ© Durrenberger (talk \| contribs) 46 edits No edit summary ← Older edit		Revision as of 19:14, 16 December 2011 view source ZoÃ© Durrenberger (talk \| contribs) 46 edits No edit summary Newer edit →
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	Moreover, invasive ''Staphylococcus aureus disease'' are often associated with the complication of endovascular infections. In order to cause this kind of complication staphylococci must first adhere to endovascular foci and colonize these tissues. One of the factors released by endothelial cells and by platelets is the von Willbrrand factor (vWF). This factor mediates the adhesion of platelets at damaged endothelial sites. It was shown that vWF binds to and also promotes the adhesion of staphylococcal cells to vWF-absorbed surfaces. It could also be demonstrated that the recognition of vWF is mediated by the staphylococcal protein A.		Moreover, invasive ''Staphylococcus aureus disease'' are often associated with the complication of endovascular infections. In order to cause this kind of complication staphylococci must first adhere to endovascular foci and colonize these tissues. One of the factors released by endothelial cells and by platelets is the von Willbrrand factor (vWF). This factor mediates the adhesion of platelets at damaged endothelial sites. It was shown that vWF binds to and also promotes the adhesion of staphylococcal cells to vWF-absorbed surfaces. It could also be demonstrated that the recognition of vWF is mediated by the staphylococcal protein A.
	Protein A defective mutants have shown reduced virulence in murine models. These observations can be explained most likely by the antiphagocytic effect of protein A binding IgG Fc fragments<ref>Hartleib, J., Köhler, N., Dickinson, R. B., Chhatwal, G. S., Sixma, J. J., M, O., Foster, T. J., et al. (2000). Protein A is the von Willebrand factor binding protein on Staphylococcus aureus, 2149-2156</ref>.		Protein A defective mutants have shown reduced virulence in murine models. These observations can be explained most likely by the antiphagocytic effect of protein A binding IgG Fc fragments<ref>Hartleib, J., Köhler, N., Dickinson, R. B., Chhatwal, G. S., Sixma, J. J., M, O., Foster, T. J., et al. (2000). Protein A is the von Willebrand factor binding protein on Staphylococcus aureus, 2149-2156</ref>.