Faculty Opinions recommendation of Staphylococcus aureus degrades neutrophil extracellular traps to promote immune cell death.

2014 ◽  
Author(s):  
Rino Rappuoli ◽  
Fabio Bagnoli
Keyword(s):  
Staphylococcus Aureus ◽  
Cell Death ◽  
Immune Cell ◽  
Neutrophil Extracellular Traps ◽  
Extracellular Traps

scholarly journals Staphylococcus aureus Degrades Neutrophil Extracellular Traps to Promote Immune Cell Death

Science ◽  
2013 ◽  
Vol 342 (6160) ◽  
pp. 863-866 ◽  
Author(s):  
V. Thammavongsa ◽  
D. M. Missiakas ◽  
O. Schneewind
Keyword(s):  
Staphylococcus Aureus ◽  
Cell Death ◽  
Immune Cell ◽  
Neutrophil Extracellular Traps ◽  
Extracellular Traps

NETosis: how vital is it?

Blood ◽  
2013 ◽  
Vol 122 (16) ◽  
pp. 2784-2794 ◽  
Author(s):  
Bryan G. Yipp ◽  
Paul Kubes
Keyword(s):  
Innate Immunity ◽  
Cell Death ◽  
Critical Role ◽  
Neutrophil Extracellular Traps ◽  
Live Cell ◽  
Extracellular Traps ◽  
Cell Death Pathway ◽  
A Cell ◽  
Net Release

Abstract In this review, we examine the evidence that neutrophil extracellular traps (NETs) play a critical role in innate immunity. We summarize how NETs are formed in response to various stimuli and provide evidence that NETosis is not universally a cell death pathway. Here we describe at least 2 different mechanisms by which NETs are formed, including a suicide lytic NETosis and a live cell or vital NETosis. We also evaluate the evidence for NETs in catching and killing pathogens. Finally, we examine how infections are related to the development of autoimmune and vasculitic diseases through unintended but detrimental bystander damage resulting from NET release.

scholarly journals ETosis: A Microbicidal Mechanism beyond Cell Death

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Anderson B. Guimarães-Costa ◽  
Michelle T. C. Nascimento ◽  
Amanda B. Wardini ◽  
Lucia H. Pinto-da-Silva ◽  
Elvira M. Saraiva
Keyword(s):  
Cell Death ◽  
Mast Cells ◽  
Cell Types ◽  
Neutrophil Extracellular Traps ◽  
Protozoan Parasites ◽  
Extracellular Milieu ◽  
Extracellular Traps ◽  
Cytoplasmic Proteins

Netosis is a recently described type of neutrophil death occurring with the release to the extracellular milieu of a lattice composed of DNA associated with histones and granular and cytoplasmic proteins. These webs, initially named neutrophil extracellular traps (NETs), ensnare and kill microorganisms. Similarly, other cell types, such as eosinophils, mast cells, and macrophages, can also dye by this mechanism; thus, it was renamed as ETosis, meaning death with release of extracellular traps (ETs). Here, we review the mechanism of NETosis/etosis, emphasizing its role in diseases caused by protozoan parasites, fungi, and viruses.

scholarly journals DEspRhigh neutrophils are associated with critical illness in COVID-19

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Joanne T. deKay ◽  
Ivette F. Emery ◽  
Jonathan Rud ◽  
Ashley Eldridge ◽  
Christine Lord ◽  
...  
Keyword(s):  
Immune Cell ◽  
Neutrophil Extracellular Traps ◽  
Extracellular Traps ◽  
Cytokines And Chemokines ◽  
Blood Smears ◽  
Secondary Tissue ◽  
Immune Cell Subpopulations ◽  
Cell Subpopulations ◽  
High Level ◽  
Negative Controls

AbstractSARS-CoV-2 infection results in a spectrum of outcomes from no symptoms to widely varying degrees of illness to death. A better understanding of the immune response to SARS-CoV-2 infection and subsequent, often excessive, inflammation may inform treatment decisions and reveal opportunities for therapy. We studied immune cell subpopulations and their associations with clinical parameters in a cohort of 26 patients with COVID-19. Following informed consent, we collected blood samples from hospitalized patients with COVID-19 within 72 h of admission. Flow cytometry was used to analyze white blood cell subpopulations. Plasma levels of cytokines and chemokines were measured using ELISA. Neutrophils undergoing neutrophil extracellular traps (NET) formation were evaluated in blood smears. We examined the immunophenotype of patients with COVID-19 in comparison to that of SARS-CoV-2 negative controls. A novel subset of pro-inflammatory neutrophils expressing a high level of dual endothelin-1 and VEGF signal peptide-activated receptor (DEspR) at the cell surface was found to be associated with elevated circulating CCL23, increased NETosis, and critical-severity COVID-19 illness. The potential to target this subpopulation of neutrophils to reduce secondary tissue damage caused by SARS-CoV-2 infection warrants further investigation.

scholarly journals Patients with recurrent PVL+-Staphylococcus aureus infections show enhanced sensitivity to PVL-mediated formation of atypical NETs

2021 ◽  
Author(s):  
Hina Jhelum ◽  
Dora Čerina ◽  
Christopher J Harbort ◽  
Andreas Lindner ◽  
Leif Gunnar Hanitsch ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Proteome Analysis ◽  
Neutrophil Extracellular Traps ◽  
Human Neutrophils ◽  
Proteinase 3 ◽  
Oxygen Species ◽  
Extracellular Traps ◽  
Enhanced Sensitivity ◽  
Microbial Toxin ◽  
Panton Valentine Leukocidin

Panton-Valentine leukocidin (PVL) is a Staphylococcus aureus (S. aureus) toxin that binds to and kills human neutrophils, resulting in the formation of neutrophil extracellular traps (NETs). Some individuals colonized with PVL-positive S. aureus (PVL-SA) suffer from recurring infections whereas others are asymptomatically colonized. We found that neutrophils from affected patients express higher levels of CD45, one of the PVL receptors, and are more susceptible to killing at a low concentration of recombinant PVL than control neutrophils. We verified that PVL induces the formation of NETs and provide genetic and pharmacological evidence that PVL-induced NET formation is independent of NADPH-oxidase and reactive oxygen species (ROS) production. Through NET proteome analysis we identified that the protein content of PVL-induced NETs is different from NETs induced by mitogen or the microbial toxin nigericin. The abundance of the proteins cathelicidin (CAMP), elastase (NE), and proteinase 3 (PRTN3) was lower on PVL-induced NETs, which were inefficient in killing S. aureus. Neutrophils from patients that suffer from recurring PVL-positive infections may be more sensitive to PVL-induced NET formation, which may impair their ability to combat the infection.

scholarly journals Degraded neutrophil extracellular traps promote the growth of Actinobacillus pleuropneumoniae

2019 ◽  
Vol 10 (9) ◽  
Author(s):  
Nicole de Buhr ◽  
Marta C. Bonilla ◽  
Jessica Pfeiffer ◽  
Silke Akhdar ◽  
Cornelia Schwennen ◽  
...  
Keyword(s):  
Immune Cell ◽  
Bacterial Species ◽  
Severe Pneumonia ◽  
Lavage Fluid ◽  
Neutrophil Extracellular Traps ◽  
Actinobacillus Pleuropneumoniae ◽  
Degraded Dna ◽  
Human Neutrophils ◽  
Extracellular Traps

Abstract Actinobacillus pleuropneumoniae (A.pp) causes severe pneumonia associated with enormous economic loss in pigs. Peracute diseased pigs die in <24 h with pneumonia. Neutrophils are the prominent innate immune cell in this infection that massively infiltrate the infected lung. Here we show that neutrophils release neutrophil extracellular traps (NETs) as response to A.pp infection. Numerous NET-markers were identified in bronchoalveolar lavage fluid (BALF) of A.pp-infected piglets in vivo, however, most NET fibers are degraded. Importantly, A.pp is able to enhance its growth rate in the presence of NETs that have been degraded by nucleases efficiently. A.pp itself releases no nuclease, but we identified host nucleases as sources that degrade NETs after A.pp infection. Furthermore, the nucleases of co-infecting pathogens like Streptococcus suis increase growth of A.pp in presence of porcine NETs. Thus, A.pp is not only evading the antimicrobial activity of NETs, A.pp is rather additionally using parts of NETs as growth factor thereby taking advantage of host nucleases as DNase1 or nucleases of co-infecting bacteria, which degrade NETs. This effect can be diminished by inhibiting the bacterial adenosine synthase indicating that degraded NETs serve as a source for NAD, which is required by A.pp for its growth. A similar phenotype was found for the human pathogen Haemophilus (H.) influenzae and its growth in the presence of human neutrophils. H. influenzae benefits from host nucleases in the presence of neutrophils. These data shed light on the detrimental effects of NETs during host immune response against certain bacterial species that require and/or efficiently take advantage of degraded DNA material, which has been provided by host nuclease or nucleases of other co-infecting bacteria, as growth source.

scholarly journals Neutrophil extracellular traps: Is immunity the second function of chromatin?

2012 ◽  
Vol 198 (5) ◽  
pp. 773-783 ◽  
Author(s):  
Volker Brinkmann ◽  
Arturo Zychlinsky
Keyword(s):  
Cell Death ◽  
Blood Cells ◽  
White Blood Cells ◽  
Neutrophil Extracellular Traps ◽  
Unique Form ◽  
Danger Signals ◽  
Extracellular Traps ◽  
Cytoplasmic Proteins ◽  
Microbial Infections

Neutrophil extracellular traps (NETs) are made of processed chromatin bound to granular and selected cytoplasmic proteins. NETs are released by white blood cells called neutrophils, maybe as a last resort, to control microbial infections. This release of chromatin is the result of a unique form of cell death, dubbed “NETosis.” Here we review our understanding of how NETs are made, their function in infections and as danger signals, and their emerging importance in autoimmunity and coagulation.

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