Project description:Streptococcus pyogenes is an obligate human pathobiont associated with many disease states. Here, we present a novel model of S. pyogenes infection using intact murine epithelium. From this model, we were able to perform RNA sequencing to evaluate the genetic changes undertaken by both the bacterium and host at 5 and 24 hours post infection. Analysis of these genomic data demonstrate that S. pyogenes undergoes significant genetic adaptation to successfully infect the murine epithelium, including changes to metabolism and activation of the Rgg2/Rgg3 quorum sensing (QS) system. Subsequent experiments demonstrate that an intact Rgg2/Rgg3 QS cascade is necessary to establish a stable superficial skin infection. Furthermore, activation of this pathway results in increased murine morbidity and increased bacterial burden on the skin. This phenotype is associated with gross changes to the murine skin, as well as histopathological evidence of inflammation. Taken together, these experiments offer a novel method to investigate S. pyogenes-epithelial interactions and demonstrate that a well-studied QS pathway is critical to a persistent infection.
Project description:In Streptococcus pyogenes, mutation of GidA results in avirulence despite the same growth rate as the wild type. To understand the basis of this effect, global transcription profiling was conducted. Keywords: Wild type vs. GidA mutant Streptococcus pyogenes
Project description:Whole genone expression profile comparing wild-type NZ131 to serR deletion mutant, grown in C-medium Mutants and interpretation are described further in the manuscript to be submitted: LaSarre and Federle, 2010. Title: Regulation and Consequence of Serine Catabolism in Streptococcus pyogenes. A two chip study using total RNA recovered from three separate wild-type cultures of Streptococcus pyogenes NZ131 and three separate mutant cultures of Streptococcus pyogenes NZ131 seR-, pooled following RNA extraction
Project description:Streptococcus pyogenes (Group A Streptococcus: GAS) is a major human pathogen that causes streptococcal pharyngitis, skin and soft-tissue infections, and life-threatening conditions such as streptococcal toxic shock syndrome (STSS). A large number of virulence-related genes are encoded on GAS genomes, which are involved in host-pathogen interaction, colonization, immune invasion, and long-term survival within hosts, causing the diverse symptoms. Here, we investigated the interaction between GAS-derived extracellular vesicles and host cells in order to reveal pathogenicity mechanisms induced by GAS infection.
Project description:Transcriptional profiling of Streptococcus pyogenes MGAS5005 cells comparing control untreated GAS cells with GAS cells exposed to 4uM heme for 1.5 h
Project description:The Antibiotic Resistant Sepsis Pathogens Framework Initiative aims to develop a framework dataset of 5 sepsis pathogens (5 strains each) using an integrated application of genomic, transcriptomic, metabolomic and proteomic technologies. The pathogens included in this initiative are: Escherichia coli, Klebsiella pneumoniae complex, Staphylococcus aureus, Streptococcus pyogenes, and Streptococcus pneumoniae. This submission pertains to Streptococcus pyogenes strains 5448, SP444, HKU419, PS003 and PS006.