The TLR2 Antagonist Staphylococcal Superantigen-Like Protein 3 Acts as a Virulence Factor to Promote Bacterial Pathogenicity in vivo

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The TLR2 Antagonist Staphylococcal Superantigen-Like Protein 3 Acts as a Virulence Factor to Promote Bacterial Pathogenicity in vivo. / Koymans, Kirsten J; Goldmann, Oliver; Karlsson, Christofer A Q; Sital, Wiedjai; Thänert, Robert; Bisschop, Adinda; Vrieling, Manouk; Malmström, Johan; Kessel, Kok P.M.; de Haas, Carla J C; van Strijp, Jos A.G.; Medina, Eva.

I: Journal of Innate Immunity, Vol. 9, 2017, s. 561-573.

Forskningsoutput: TidskriftsbidragArtikel i vetenskaplig tidskrift

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Koymans, KJ, Goldmann, O, Karlsson, CAQ, Sital, W, Thänert, R, Bisschop, A, Vrieling, M, Malmström, J, Kessel, KPM, de Haas, CJC, van Strijp, JAG & Medina, E 2017, 'The TLR2 Antagonist Staphylococcal Superantigen-Like Protein 3 Acts as a Virulence Factor to Promote Bacterial Pathogenicity in vivo', Journal of Innate Immunity, vol. 9, s. 561-573. https://doi.org/10.1159/000479100

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Author

Koymans, Kirsten J ; Goldmann, Oliver ; Karlsson, Christofer A Q ; Sital, Wiedjai ; Thänert, Robert ; Bisschop, Adinda ; Vrieling, Manouk ; Malmström, Johan ; Kessel, Kok P.M. ; de Haas, Carla J C ; van Strijp, Jos A.G. ; Medina, Eva. / The TLR2 Antagonist Staphylococcal Superantigen-Like Protein 3 Acts as a Virulence Factor to Promote Bacterial Pathogenicity in vivo. I: Journal of Innate Immunity. 2017 ; Vol. 9. s. 561-573.

RIS

TY - JOUR

T1 - The TLR2 Antagonist Staphylococcal Superantigen-Like Protein 3 Acts as a Virulence Factor to Promote Bacterial Pathogenicity in vivo

AU - Koymans, Kirsten J

AU - Goldmann, Oliver

AU - Karlsson, Christofer A Q

AU - Sital, Wiedjai

AU - Thänert, Robert

AU - Bisschop, Adinda

AU - Vrieling, Manouk

AU - Malmström, Johan

AU - Kessel, Kok P.M.

AU - de Haas, Carla J C

AU - van Strijp, Jos A.G.

AU - Medina, Eva

N1 - © 2017 S. Karger AG, Basel.

PY - 2017

Y1 - 2017

N2 - Toll-like receptor (TLR) signaling is important in the initiation of immune responses and subsequent instigation of adaptive immunity. TLR2 recognizes bacterial lipoproteins and plays a central role in the host defense against bacterial infections, including those caused by Staphylococcus aureus. Many studies have demonstrated the importance of TLR2 in murine S. aureus infection. S. aureus evades TLR2 activation by secreting two proteins, staphylococcal superantigen-like protein 3 (SSL3) and 4 (SSL4). In this study, we demonstrate that antibodies against SSL3 and SSL4 are found in healthy individuals, indicating that humans are exposed to these proteins during S. aureus colonization or infection. To investigate the TLR2-antagonistic properties of SSL3 and SSL4, we compared the infection with wild-type and SSL3/4 knockout S. aureus strains in an intravenous murine infection model. Direct evaluation of the contribution of SSL3/4 to infection pathogenesis was hindered by the fact that the SSLs were not expressed in the murine system. To circumvent this limitation, an SSL3-overproducing strain (pLukM-SSL3) was generated, resulting in constitutive expression of SSL3. pLukM-SSL3 exhibited increased virulence compared to the parental strain in a murine model that was found to be TLR2 dependent. Altogether, these data indicate that SSL3 contributes to S. aureus virulence in vivo.

AB - Toll-like receptor (TLR) signaling is important in the initiation of immune responses and subsequent instigation of adaptive immunity. TLR2 recognizes bacterial lipoproteins and plays a central role in the host defense against bacterial infections, including those caused by Staphylococcus aureus. Many studies have demonstrated the importance of TLR2 in murine S. aureus infection. S. aureus evades TLR2 activation by secreting two proteins, staphylococcal superantigen-like protein 3 (SSL3) and 4 (SSL4). In this study, we demonstrate that antibodies against SSL3 and SSL4 are found in healthy individuals, indicating that humans are exposed to these proteins during S. aureus colonization or infection. To investigate the TLR2-antagonistic properties of SSL3 and SSL4, we compared the infection with wild-type and SSL3/4 knockout S. aureus strains in an intravenous murine infection model. Direct evaluation of the contribution of SSL3/4 to infection pathogenesis was hindered by the fact that the SSLs were not expressed in the murine system. To circumvent this limitation, an SSL3-overproducing strain (pLukM-SSL3) was generated, resulting in constitutive expression of SSL3. pLukM-SSL3 exhibited increased virulence compared to the parental strain in a murine model that was found to be TLR2 dependent. Altogether, these data indicate that SSL3 contributes to S. aureus virulence in vivo.

U2 - 10.1159/000479100

DO - 10.1159/000479100

M3 - Article

VL - 9

SP - 561

EP - 573

JO - Journal of Innate Immunity

T2 - Journal of Innate Immunity

JF - Journal of Innate Immunity

SN - 1662-811X

ER -