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Molecular insight into invasive group A streptococcal disease

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TLDR
The virulence factors and newly discovered molecular events that mediate the in vivo changes from non-invasive GAS serotype M1T1 to the invasive phenotype are described and the invasive-disease trigger for non-M1 GAS is reviewed.
Abstract
Streptococcus pyogenes is also known as group A Streptococcus (GAS) and is an important human pathogen that causes considerable morbidity and mortality worldwide. The GAS serotype M1T1 clone is the most frequently isolated serotype from life-threatening invasive (at a sterile site) infections, such as streptococcal toxic shock-like syndrome and necrotizing fasciitis. Here, we describe the virulence factors and newly discovered molecular events that mediate the in vivo changes from non-invasive GAS serotype M1T1 to the invasive phenotype, and review the invasive-disease trigger for non-M1 GAS. Understanding the molecular basis and mechanism of initiation for streptococcal invasive disease may expedite the discovery of novel therapeutic targets for the treatment and control of severe invasive GAS diseases.

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Infection-induced NETosis is a dynamic process involving neutrophil multitasking in vivo

TL;DR: Early in infection NETosis involves neutrophils that do not undergo lysis and retain the ability to multitask, and a requirement for both Toll-like receptor 2 and complement-mediated opsonization tightly regulated NET release.
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Disease Manifestations and Pathogenic Mechanisms of Group A Streptococcus

TL;DR: Genomic and molecular analyses have now characterized a large number of GAS virulence determinants, many of which exhibit overlap and redundancy in the processes of adhesion and colonization, innate immune resistance, and the capacity to facilitate tissue barrier degradation and spread within the human host.
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Staphylococcal and Streptococcal Superantigen Exotoxins

TL;DR: The review discusses the major known and possible human disease associations with superantigens, including associations with toxic shock syndromes, atopic dermatitis, pneumonia, infective endocarditis, and autoimmune sequelae to streptococcal illnesses.
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Structure and function of the human skin microbiome

TL;DR: The present understanding of the function of microbe-host interactions on the skin is summarized and some unique features that distinguish skin commensal organisms from pathogenic microbes are highlighted.
References
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Journal ArticleDOI

Neutrophil extracellular traps kill bacteria

TL;DR: It is described that, upon activation, neutrophils release granule proteins and chromatin that together form extracellular fibers that bind Gram-positive and -negative bacteria, which degrade virulence factors and kill bacteria.
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The global burden of group A streptococcal diseases

TL;DR: The need to reinforce current control strategies, develop new primary prevention strategies, and collect better data from developing countries for most diseases is highlighted, as GAS is an important cause of morbidity and mortality.
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Pathogenesis of Group A Streptococcal Infections

TL;DR: Group A streptococci are model extracellular gram-positive pathogens responsible for pharyngitis, impetigo, rheumatic fever, and acute glomerulonephritis, and an emerging theme is the dichotomy between skin and throat strains in their epidemiology and genetic makeup.
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ECM and cell surface proteolysis: regulating cellular ecology.

TL;DR: Understanding the mechanisms by which pericellular proteinases are regulated and activated, the nature of their molecular targets, and how adhesion and proteolysis are integrated will provide exciting avenues for investigation over the next few years.
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Autophagy defends cells against invading group A Streptococcus.

TL;DR: It is found that the autophagic machinery could effectively eliminate pathogenic group A Streptococcus within nonphagocytic cells within autophagy-deficient Atg5–/– cells.
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