The IL-8 Protease SpyCEP/ScpC of Group A Streptococcus Promotes Resistance to Neutrophil Killing

Zinkernagel, Annelies S.; Timmer, Anjuli M.; Pence, Morgan A.; Locke, Jeffrey B.; Buchanan, John T.; Turner, Claire E.; Mishalian, Inbal; Sriskandan, Shiranee; Hanski, Emanuel; Nizet, Victor

doi:10.1016/j.chom.2008.07.002

Cited by 163 publications

(198 citation statements)

References 47 publications

(63 reference statements)

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“…Research over the past decade has now shown that three comparable mechanisms are also employed by pathogenic bacteria, viruses, and parasites: inhibition of NETs release, degradation of NETs, and resistance to NETs killing (Figure 2). Perhaps the best example of this is GAS, which has evolved mechanisms to evade NETs using all three of these strategies (10,(14)(15)(16)(17).…”

Section: Pathogen Evasion Of Netsmentioning

confidence: 99%

Evasion of Neutrophil Extracellular Traps by Respiratory Pathogens

Storisteanu¹,

Pocock²,

Cowburn

et al. 2017

Am J Respir Cell Mol Biol

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The release of neutrophil extracellular traps (NETs) is a major immune mechanism intended to capture pathogens. These histoneand protease-coated DNA structures are released by neutrophils in response to a variety of stimuli, including respiratory pathogens, and have been identified in the airways of patients with respiratory infection, cystic fibrosis, acute lung injury, primary graft dysfunction, and chronic obstructive pulmonary disease. NET production has been demonstrated in the lungs of mice infected with Staphylococcus aureus, Klebsiella pneumoniae, and Aspergillus fumigatus. Since the discovery of NETs over a decade ago, evidence that "NET evasion" might act as an immune protection strategy among respiratory pathogens, including group A Streptococcus, Bordetella pertussis, and Haemophilus influenzae, has been growing, with the majority of these studies being published in the past 2 years. Evasion strategies fall into three main categories: inhibition of NET release by down-regulating host inflammatory responses; degradation of NETs using pathogen-derived DNases; and resistance to the microbicidal components of NETs, which involves a variety of mechanisms, including encapsulation. Hence, the evasion of NETs appears to be a widespread strategy to allow pathogen proliferation and dissemination, and is currently a topic of intense research interest. This article outlines the evidence supporting the three main strategies of NET evasion-inhibition, degradation, and resistance-with particular reference to common respiratory pathogens.

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Section: Pathogen Evasion Of Netsmentioning

confidence: 99%

Evasion of Neutrophil Extracellular Traps by Respiratory Pathogens

Storisteanu¹,

Pocock²,

Cowburn

et al. 2017

Am J Respir Cell Mol Biol

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“…The presence and kinetics of free circulating neutrophilderived DNA/NETs appear to serve as a useful marker of sepsis disease severity and multiple organ failure in patients following multiple traumas [84]. Specific bacterial products, such as the surface expressed M protein of S. pyogenes, or host chemokines, such as IL-8, can induce the production of NETs [85,86]. It is now recognized that certain leading leading bacterial pathogens, including Streptococcus pneumoniae and S. pyogenes, express broadspectrum DNAses that have recently been shown to dissolve NETs, allowing pathogen to escape entrapment and spread to produce systemic infection in the host into the host [87][88][89].…”

Section: Induction Of Neutrophil Extracellular Trap-associated Cell Dmentioning

confidence: 99%

Cell death during sepsis: integration of disintegration in the inflammatory response to overwhelming infection

Silva

Nizet

2009

Apoptosis

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Sepsis is a major health problem and a leading cause of death worldwide. In recent years, a crescendo of attention has been directed to the mechanisms of cell death that develop during this disease, since these are viewed as important contributors to the proinflammatory and antiinflammatory responses associated with poor outcome. Here we discuss mechanisms of cell death evident severe bacterial infection and sepsis including necrosis, apoptosis, pyroptosis, and extracellular trap-associated neutrophil death, with a particular emphasis on lymphocyte apoptosis and its contribution to the immunosuppressed phenotype of late sepsis. Individual bacterial pathogens express virulence factors that modulate cell death pathways and influence the sepsis phenotype. A greater knowledge of cell death pathways in sepsis informs the potential for future therapies designed to ameliorate immune dysfunction in this syndrome.

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“…While several studies have been conducted on S. iniae, attention to date has mainly focused on the so-called virulence factors SiM protein [2,5]. interleukin-8 protease [6], streptolysin S [7]. C5a peptidase [8], capsule [1,[9][10][11].…”

Section: Introductionmentioning

confidence: 99%

Comparative genome analysis of Streptococcus iniae DX09 reveals new insights into niche adaptation and competitive host colonisation ability

Liu¹,

Wang²,

Wang³

2017

Oncotarget

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Streptococcus iniae is a significant pathogen in a variety of marine and freshwater cultured fish species. Previous investigations on S. iniae have been limited to a single virulence gene or genome. However, different strains are associated with varying pathogenicity and niche adaptation properties. For comprehensive characterization of the genetic variations in S. iniae, whole-genome sequencing of S. iniae DX09 (isolated from diseased catfish) was performed and comparative genome analysis with eight S. iniae strains conducted to determine the virulence evolution patterns. Comparative analysis of all sequenced S. iniae revealed genome-genome variations, mainly in two plasticity zones, within genes encoding specific functions, such as the Ess/type VII secretion system and phosphoenolpyruvate-carbohydrate phosphotransferase system, reflecting adaptation to colonisation of specific host habitats. The plasticity zones analyzed in the S. iniae genome may be a paradigm rather than a unique combination of horizontal gene transfer and underlie the emergence of pathogenic Gram-positive bacteria.

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The IL-8 Protease SpyCEP/ScpC of Group A Streptococcus Promotes Resistance to Neutrophil Killing

Cited by 163 publications

References 47 publications

Evasion of Neutrophil Extracellular Traps by Respiratory Pathogens

Evasion of Neutrophil Extracellular Traps by Respiratory Pathogens

Cell death during sepsis: integration of disintegration in the inflammatory response to overwhelming infection

Comparative genome analysis of Streptococcus iniae DX09 reveals new insights into niche adaptation and competitive host colonisation ability

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