pyogenes, congruent with general cellular processes such as differentiation and proliferation. We further found several virulence factors including hyaluronan synthase, Sic1, Isp, SagF, SagG, ScfAB-operon, Fba and genes upstream and downstream of EndoS along with bacterial housekeeping genes interacting with the human stress and immune response in various subnetworks between host and pathogen.Īt the population level, we found aetiology-dependent responses showing the potential modes of entry and immune evasion strategies employed by S. pyogenes in this subnetwork were characterised by cellular response to cytokines. pyogenes, Porphyromonas asaccharolytica and Escherichia coli ) and host genes. The polymicrobial network consisted of several significant associations between different species ( S. pyogenes mono-microbial subnetwork was enriched with host genes annotated with involved in cytokine production and regulation of response to stress. NSTI type-specific responses in the host were uncovered. In this study, we built interactomes at both the population and individual levels consisting of host-pathogen interactions inferred from dual RNA-Seq gene transcriptomic profiles of the biopsies from NSTI patients. However, the underlying pathogenic mechanisms in this heterogeneous group remain elusive. These infections are rare and are associated with high mortality rates. Necrotising soft tissue infections (NSTIs) are rapidly progressing bacterial infections usually caused by either several pathogens in unison (polymicrobial infections) or Streptococcus pyogenes (mono-microbial infection).
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