DNase Expression Allows the Pathogen Group A Streptococcus to Escape Killing in Neutrophil Extracellular Traps

  title={DNase Expression Allows the Pathogen Group A Streptococcus to Escape Killing in Neutrophil Extracellular Traps},
  author={John T. Buchanan and A J Simpson and Ramy Karam Aziz and George Y. Liu and Sascha A. Kristian and Malak Kotb and James R. Feramisco and Victor Nizet},
  journal={Current Biology},

Nuclease Expression by Staphylococcus aureus Facilitates Escape from Neutrophil Extracellular Traps

Targeted mutagenesis shows that S. aureus nuclease promotes resistance against NET-mediated antimicrobial activity of neutrophils and contributes to disease pathogenesis in vivo.

Candida Extracellular Nucleotide Metabolism Promotes Neutrophils Extracellular Traps Escape

It is shown that, during neutrophils-Candida interaction, when NETs formation and release are triggered, NETs digestion occurs and this process of NETs disruption promoted by yeast cells was prevented by ammonium tetrathiomolybdate (TTM), a 3′NT/NU inhibitor.

M1 Protein Allows Group A Streptococcal Survival in Phagocyte Extracellular Traps through Cathelicidin Inhibition

Increased resistance to host cathelicidin and killing within phagocyte extracellular traps contribute to the propensity of M1 GAS strains to produce invasive infections.

The intriguing host innate immune response: novel anti-parasitic defence by neutrophil extracellular traps

Special attention will be given to NET-associated mechanisms by which parasites, in particular apicomplexa, might be hampered in their ability to reproduce within the host cell and complete the life cycle.

Neutrophil Extracellular Traps in Infectious Human Diseases

This chapter focuses on possible pathways involved in the release of NETs and summarizes the current knowledge on triggers of this process during bacterial, fungal, protozoan, and viral infections, and considers the mechanisms used by microorganisms to evade NET‐killing activity.

Interaction of Bacterial Exotoxins with Neutrophil Extracellular Traps: Impact for the Infected Host

The contemporary research on the interaction of bacterial exotoxins with neutrophils that modulate NET production is summarized, focusing particular attention on consequences for the host.

DNase Sda1 Allows Invasive M1T1 Group A Streptococcus to Prevent TLR9-Dependent Recognition

GAS Sda1 suppressed both the TLR9-mediated innate immune response and macrophage bactericidal activity, demonstrating a novel mechanism of bacterial innate immune evasion based on autodegradation of CpG-rich DNA by a bacterial DNase.

Neutrophil Extracellular Traps: As Antimicrobial Peptides

  • Q. Ann
  • Biology, Medicine
    Oral Rehabilitation and Dentistry
  • 2019
Genetic shortcomings in neutrophils with respect to their chemotaxis, migration and phagocytosis become evident as severe forms of periodontitis, thus highlighting their role in innate immunity.

To Trap a Pathogen: Neutrophil Extracellular Traps and Their Role in Mucosal Epithelial and Skin Diseases

The role of NETs in different infectious and inflammatory diseases of the mucosal epithelia and skin is examined to understand its function and regulation in health and disease.



Extracellular deoxyribonuclease made by group A Streptococcus assists pathogenesis by enhancing evasion of the innate immune response.

It is concluded that extracellular DNase activity made by GAS contributes to disease progression, thereby resolving a long-standing question in bacterial pathogenesis research.

Neutrophil Extracellular Traps Kill Bacteria

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.

Mutational analysis of the group A streptococcal operon encoding streptolysin S and its virulence role in invasive infection

It is concluded that all genetic components of the sag operon are required for expression of functional SLS, an important virulence factor in the pathogenesis of invasive M1T1 GAS infection.

Alanylation of teichoic acids protects Staphylococcus aureus against Toll-like receptor 2-dependent host defense in a mouse tissue cage infection model.

It is indicated that alanylated teichoic acids contribute to virulence of S. aureus, and TLR2 mediates host defense, which partly targets alanylation of cell envelope te Jerichoic acids.

Investigation of a Novel DNase of Streptococcus suis Serotype 2

Reverse transcription-PCR experiments revealed that ssnA is expressed throughout all stages of S. suis growth, and Western blots with porcine anti-S.

How neutrophils kill microbes.

  • A. Segal
  • Biology
    Annual review of immunology
  • 2005
Killing was previously believed to be accomplished by oxygen free radicals and other reactive oxygen species generated by the NADPH oxidase, and by oxidized halides produced by myeloperoxidase, but this is incorrect.

Blood-brain barrier invasion by group B Streptococcus depends upon proper cell-surface anchoring of lipoteichoic acid.

It is suggested that LTA expression on the GBS surface plays a role in bacterial interaction with BBB endothelium and the pathogenesis of neonatal meningitis.

Molecular Genetic Analysis of a Group A Streptococcus Operon Encoding Serum Opacity Factor and a Novel Fibronectin-Binding Protein, SfbX

Targeted in-frame allelic-exchange mutagenesis, complementation, and heterologous-expression studies found that serum opacification is encoded by sof alone and that sfbX encodes a fibronectin-binding function.

Evolutionary origin and emergence of a highly successful clone of serotype M1 group a Streptococcus involved multiple horizontal gene transfer events.

Virtual identity in the 36-kb region present in contemporary serotypes M1 and M12 isolates suggests that a serotype M12 strain served as the donor of this region and was associated with significantly increased production of SLO and NADase.