The Experts below are selected from a list of 21819 Experts worldwide ranked by ideXlab platform

Andreas Peschel - One of the best experts on this subject based on the ideXlab platform.

  • toll like Receptor 2 activation depends on lipopeptide shedding by bacterial surfactants
    Nature Communications, 2016
    Co-Authors: Dennis Hanzelmann, Mirita Franzwachtel, Tobias Hertlein, Stefan Stevanovic, Boris Macek, Christiane Wolz, Friedrich Gotz, Michael Otto, Dorothee Kretschmer, Andreas Peschel
    Abstract:

    Sepsis caused by Gram-positive bacterial pathogens is a major fatal disease but its molecular basis remains elusive. Toll-Like Receptor 2 (TLR2) has been implicated in the orchestration of inflammation and sepsis but its role appears to vary for different pathogen species and clones. Accordingly, Staphylococcus aureus clinical isolates differ substantially in their capacity to activate TLR2. Here we show that strong TLR2 stimulation depends on high-level production of phenol-soluble modulin (PSM) peptides in response to the global virulence activator Agr. PSMs are required for mobilizing lipoproteins, the TLR2 agonists, from the staphylococcal cytoplasmic membrane. Notably, the course of sepsis caused by PSM-deficient S. aureus is similar in wild-type and TLR2-deficient mice, but TLR2 is required for protection of mice against PSM-producing S. aureus. Thus, a crucial role of TLR2 depends on agonist release by bacterial surfactants. Modulation of this process may lead to new therapeutic strategies against Gram-positive infections. The role played by human protein TLR2 in inflammation and sepsis varies for different bacterial pathogens. Here, Hanzelmann et al. show that the differential abilities of Staphylococcus aureusstrains to activate TLR2 depend on their production of peptides that release lipoproteins known to act as TLR2 agonists.

Ivo G Boneca - One of the best experts on this subject based on the ideXlab platform.

  • Toll-Like Receptor 2-dependent bacterial sensing does not occur via peptidoglycan recognition
    EMBO Reports, 2004
    Co-Authors: Leonardo H. Travassos, Catherine Werts, Didier Blanot, Dana J. Philpott, Stephen E. Girardin, Marie Anne Nahori, Ivo G Boneca
    Abstract:

    Toll-Like Receptor 2 (TLR2) has been shown to recognize several classes of pathogen-associated molecular patterns including peptidoglycan (PG). However, studies linking PG with TLR2 recognition have relied mainly on the use of commercial Staphylococcus aureus PG and have not addressed TLR2 recognition of other PG types. Using highly purified PGs from eight bacteria (Escherichia coli, Pseudomonas aeruginosa, Yersinia pseudotuberculosis, Helicobacter pylori, Bacillus subtilis, Listeria monocytogenes, Streptococcus pneumoniae and S. aureus), we show that these PGs are not sensed through TLR2, TLR2/1 or TLR2/6. PG sensing is lost after removal of lipoproteins or lipoteichoic acids (LTAs) from Gram-negative and Gram-positive cell walls, respectively. Accordingly, purified LTAs are sensed synergistically through TLR2/1. Finally, we show that elicited peritoneal murine macrophages do not produce tumour necrosis factor-alpha or interleukin-6 in response to purified PGs, suggesting that PG detection is more likely to occur intracellularly (through Nod1/Nod2) rather than from the extracellular compartment.

Dennis Hanzelmann - One of the best experts on this subject based on the ideXlab platform.

  • toll like Receptor 2 activation depends on lipopeptide shedding by bacterial surfactants
    Nature Communications, 2016
    Co-Authors: Dennis Hanzelmann, Mirita Franzwachtel, Tobias Hertlein, Stefan Stevanovic, Boris Macek, Christiane Wolz, Friedrich Gotz, Michael Otto, Dorothee Kretschmer, Andreas Peschel
    Abstract:

    Sepsis caused by Gram-positive bacterial pathogens is a major fatal disease but its molecular basis remains elusive. Toll-Like Receptor 2 (TLR2) has been implicated in the orchestration of inflammation and sepsis but its role appears to vary for different pathogen species and clones. Accordingly, Staphylococcus aureus clinical isolates differ substantially in their capacity to activate TLR2. Here we show that strong TLR2 stimulation depends on high-level production of phenol-soluble modulin (PSM) peptides in response to the global virulence activator Agr. PSMs are required for mobilizing lipoproteins, the TLR2 agonists, from the staphylococcal cytoplasmic membrane. Notably, the course of sepsis caused by PSM-deficient S. aureus is similar in wild-type and TLR2-deficient mice, but TLR2 is required for protection of mice against PSM-producing S. aureus. Thus, a crucial role of TLR2 depends on agonist release by bacterial surfactants. Modulation of this process may lead to new therapeutic strategies against Gram-positive infections. The role played by human protein TLR2 in inflammation and sepsis varies for different bacterial pathogens. Here, Hanzelmann et al. show that the differential abilities of Staphylococcus aureusstrains to activate TLR2 depend on their production of peptides that release lipoproteins known to act as TLR2 agonists.

Juana L De Diego - One of the best experts on this subject based on the ideXlab platform.

Massimiliano M. Corsi Romanelli - One of the best experts on this subject based on the ideXlab platform.

  • Toll-Like Receptor 2 in serum: A potential diagnostic marker of prosthetic joint infection?
    Journal of Clinical Microbiology, 2014
    Co-Authors: Emanuela Galliera, Monica Gioia Marazzi, Lucia Salcito, Christian Vassena, Lorenzo Drago, Carlo Romano, Massimiliano M. Corsi Romanelli
    Abstract:

    Prosthetic joint infection (PJI) is a severe complication of arthroplasty and is still lacking diagnostic gold standards. PJI patients display high Toll-Like Receptor 2 (TLR2) serum levels, correlating with canonical inflammatory markers (C-reactive protein [CRP], interleukin 6 [IL-6], tumor necrosis factor alpha [TNF-α], and IL-1). Therefore, TLR2 serum levels could be considered a new potential diagnostic tool in the early detection of PJI.