Specific immuno capturing of the Staphylococcal superantigen toxic-shock syndrome toxin-1 in plasma

Toxic‐shock syndrome is primarily caused by the Toxic‐shock syndrome toxin 1 (TSST‐1), which is secreted by the Gram‐positive bacterium Staphylococcus aureus. The toxin belongs to a family of superantigens (SAgs) which exhibit several shared biological properties, including the induction of massive...

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Published inBiotechnology and bioengineering Vol. 104; no. 1; pp. 143 - 151
Main Authors Adams, Hendrik, Brummelhuis, Walter, Maassen, Bram, van Egmond, Nathalie, Khattabi, Mohamed El, Detmers, Frank, Hermans, Pim, Braam, Branko, Stam, Jord, Verrips, Theo
Format Journal Article
LanguageEnglish
Published Hoboken Wiley Subscription Services, Inc., A Wiley Company 01.09.2009
Wiley
Wiley Subscription Services, Inc
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Summary:Toxic‐shock syndrome is primarily caused by the Toxic‐shock syndrome toxin 1 (TSST‐1), which is secreted by the Gram‐positive bacterium Staphylococcus aureus. The toxin belongs to a family of superantigens (SAgs) which exhibit several shared biological properties, including the induction of massive cytokine release and Vβ‐specific T‐cell proliferation. In this study we explored the possibility to use monoclonal Variable domains of Llama Heavy‐chain antibodies (VHH) in the immuno capturing of TSST‐1 from plasma. Data is presented that the selected VHHs are highly specific for TSST‐1 and can be efficiently produced in large amounts in yeast. In view of affinity chromatography, the VHHs are easily coupled to beads, and are able to deplete TSST‐1 from plasma at very low, for example, pathologically relevant, concentrations. When spiked with 4 ng/mL TSST‐1 more than 96% of TSST‐1 was depleted from pig plasma. These data pave the way to further explore application of high‐affinity columns in the specific immuno depletion of SAgs in experimental sepsis models and in sepsis in humans. Biotechnol. Bioeng. 2009; 104: 143–151 © 2009 Wiley Periodicals, Inc.
Bibliography:SenterNovem, The Netherlands - No. TSGE 3131
ArticleID:BIT22365
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ISSN:0006-3592
1097-0290
DOI:10.1002/bit.22365