Webbläsaren som du använder stöds inte av denna webbplats. Alla versioner av Internet Explorer stöds inte längre, av oss eller Microsoft (läs mer här: * https://www.microsoft.com/en-us/microsoft-365/windows/end-of-ie-support).

Var god och använd en modern webbläsare för att ta del av denna webbplats, som t.ex. nyaste versioner av Edge, Chrome, Firefox eller Safari osv.

The N-terminal of thrombospondin-1 is essential for coagulase-negative staphylococcal binding

Författare

  • Naoko Yanagisawa
  • Dai-Qing Li
  • Åsa Ljungh

Summary, in English

Bacterial binding was studied to determine whether thrombospondin-1 (TSP) acts as a ligand in attachment of coagulase-negative staphylococci (CNS). Twenty-five of 27 CNS strains bound soluble TSP. Staphylococcus epidermidis J9P bound 125I-labelled TSP in a dose-dependent manner. Scatchard plot analysis of the binding of TSP by strain J9P revealed two Kd values of 6.4x10-95muM and 2.9x10-85muM. The binding structures of strain J9P were sensitive to protease and were resistant to heat treatment. Unlabelled TSP and recombinant von Willebrand factor inhibited binding of TSP by strain J9P, but other proteins or monosaccharides did not. Heparin inhibited binding of TSP to strain J9P and two other S. epidermidis strains, BD5703 and BD969. Fusion proteins of the type 1 repeats, type 2 repeats, type 3 repeats and C-terminal domain of TSP or the synthetic Arg-Gly-Asp peptide did not inhibit binding of TSP to bacteria. TSP promoted adhesion of S. epidermidis strains when it was immobilised on polymer surfaces. These results indicate that the specific interaction between CNS and TSP may contribute to bacterial adhesion on biomaterial surfaces. The N-terminal heparin-binding domain of TSP appears to be the major region for recognition by CNS.

Publiceringsår

2001

Språk

Engelska

Sidor

712-719

Publikation/Tidskrift/Serie

Journal of Medical Microbiology

Volym

50

Issue

8

Dokumenttyp

Artikel i tidskrift

Förlag

Lippincott Williams & Wilkins

Ämne

  • Microbiology in the medical area

Status

Published

Forskningsgrupp

  • Diabetes - Islet Patophysiology

ISBN/ISSN/Övrigt

  • ISSN: 0022-2615