Frontiers in Microbiology · 2014 · 12 citations · 39 references
Life SciencesImmunologyInfectious DiseasesHost-pathogen InteractionsInflammationInnate ImmunityBacterial PathogenesisBacterial Virulence FactorsHost Immune ResponseInnate Immune ActivationInnate Immune ResponsePathogen Virulence FactorsHost Defense Against Bacterial InfectionInnate Immune EffectorsInnate Immune FunctionInnate Immune Recognition Of BacteriaInnate Immunity PathwaysLivestock-associated Methicillin-resistant Staphylococcus AureusNf-kappa B-dependent TranscriptionToll-like Receptor-mediated Innate Immune Response
Staphylococcus aureus, sequence type (ST) 398, is an emerging pathogen and the leading cause of livestock-associated methicillin-resistant S. aureus infections in Europe and North America. This strain is characterized by high promiscuity in terms of host-species and also lacks several traditional S. aureus virulence factors. This does not, however, explain the apparent ease with which it crosses species-barriers. Recently, TIR-domain containing proteins (Tcps) which inhibit the innate immune response were identified in some Gram-negative bacteria. Here we report the presence of two proteins, S. aureus TIR-like Protein 1 (SaTlp1) and S. aureus TIR-like Protein 2 (SaTlp2), expressed by ST398 which contain domain of unknown function 1863 (DUF1863), similar to the Toll/IL-1 receptor (TIR) domain. In contrast to the Tcps in Gram-negative bacteria, our data suggest that SaTlp1 and SaTlp2 increase activation of the transcription factor NF-κB as well as downstream pro-inflammatory cytokines and immune effectors. To assess the role of both proteins as potential virulence factors knock-out mutants were created. These showed a slightly enhanced survival rate in a murine infectious model compared to the wild-type strain at one dose. Our data suggest that both proteins may act as factors contributing to the enhanced ability of ST398 to cross species-barriers.
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Inference of Macromolecular Assemblies from Crystalline State
Evgeny Krissinel, Kim Henrick · Journal of Molecular Biology · 2007 · 10.4K citations · Full text