Heterogeneity of host TLR2 stimulation by Staphylocoocus aureus isolates

PLoS One. 2014 May 8;9(5):e96416. doi: 10.1371/journal.pone.0096416. eCollection 2014.

Abstract

High lipoprotein expression and potent activation of host Toll-like receptor-2 (TLR2) are characteristic features of the staphylococcal species. Expression of TLR2 in the host is important for clearance of Staphylococcus aureus infection and host survival. Thus, we hypothesized that bacterial regulation of its intrinsic TLR2-stimulatory capacity could represent a means for immune evasion or host adaptation. We, therefore, compared clinical S. aureus isolates in regards to their TLR2 activation potential and assessed the bacterial factors that modulate TLR2-mediated recognition. S. aureus isolates displayed considerable variability in TLR2-activity with low to absent TLR2-activity in 64% of the isolates tested (68/106). Notably, strain-specific TLR2-activity was independent of the strain origin, e.g. no differences were found between strains isolated from respiratory specimen from cystic fibrosis patients or those isolated from invasive disease specimen. TLR2-activity correlated with protein A expression but not with the agr status. Capsule expression and small colony variant formation had a negative impact on TLR2-activity but any disruption of cell wall integrity enhanced TLR2 activation. Altogether, heterogeneity in host TLR2-activity reflects differences in metabolic activity and cell wall synthesis and/or remodeling.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Wall / immunology
  • Cell Wall / metabolism
  • HEK293 Cells
  • Humans
  • Immunity, Innate
  • Lipoproteins / metabolism
  • Staphylococcal Infections / immunology
  • Staphylococcal Infections / microbiology*
  • Staphylococcus aureus / isolation & purification
  • Staphylococcus aureus / metabolism*
  • Toll-Like Receptor 2 / metabolism*

Substances

  • Lipoproteins
  • Toll-Like Receptor 2

Grants and funding

DH received a grant from the University of Damaskus, Syria. IBD received funding from the German Research Association (DFG) Priority program “IMMUNOBONE” grant RI-707/8-1, the ARGUS Stiftung, the Medical faculty of the University of Heidelberg, Germany (Olympia Morata program) and the Medical faculty of the University Hospital Bonn (BONFOR program. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.