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- Rydén, Cecilia, et al.
(author)
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Identification of the binding sequence for Staphylococcus aureus in bone sialoprotein
- 1997
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In: Biochemical Journal. - 0264-6021 .- 1470-8728. ; 327:3, s. 825-829
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Journal article (peer-reviewed)abstract
- Bone sialoprotein is a glycoprotein of the bone and dentine extracellular matrix. This protein consists of 320 amino acids, of which 25% are glutamic and aspartic acid residues. Sialic acid, containing oligosaccharides and tyrosine sulphate residues, supplies additional polyanionic properties. Staphylococcal cells, isolated from patients suffering from infection of bone tissue, bind the bone-derived sialoprotein, an interaction which is specifically inhibited by the recombinant bone sialoprotein core protein. We have previously shown that the 150 N-terminal amino acid residues of bone sialoprotein are responsible for the binding to staphylococcal cells. By using recombinant deleted variants of bone sialoprotein and synthetic peptides, we have now localized the staphylococcal binding site to less than 10 residues within the N-terminal part of the protein.
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- Verdrengh, M, et al.
(author)
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Integrin-associated protein (IAP)-deficient mice are less susceptible to developing Staphylococcus aureus induced arthritis
- 1999
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In: Microbes and infection. - 1286-4579 .- 1769-714X. ; 1:10, s. 745-751
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Journal article (peer-reviewed)abstract
- The integrin-associated protein (IAP) has been shown to function in a signaling complex with β3 integrins, influencing the migration of phagocytic cells into inflamed tissues. We have previously shown that gene-targeted mice deficient for IAP succumbed to peritonitis when inoculated with Gram-negative bacteria. The aim of this study was to assess the role of IAP in our recently established model of haematogenously induced Staphylococcus aureus septicaemia and arthritis. In this model, neutrophils play a crucial role in the early phase of the infection. Mice lacking IAP and congenic controls were intravenously inoculated with S. aureus LS-1. The IAP-/- mice were resistant to developing clinical signs of arthritis compared with their IAP-expressing littermates. The clinical findings were corroborated by histopathological evaluation indicating that the IAP-/- mice had less cartilage and bone destruction in the joints. We believe that a delayed migration of leukocytes into the joints of mice lacking IAP expression leads to decreased susceptibility to develop S. aureus-induced arthritis.
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