scholarly journals The humoral pattern recognition receptor PTX3 is stored in neutrophil granules and localizes in extracellular traps

2007 ◽  
Vol 204 (4) ◽  
pp. 793-804 ◽  
Author(s):  
Sébastien Jaillon ◽  
Giuseppe Peri ◽  
Yves Delneste ◽  
Isabelle Frémaux ◽  
Andrea Doni ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Neutrophil Extracellular Traps ◽  
Toll Like Receptor ◽  
Myeloid Dendritic Cells ◽  
Opsonic Activity ◽  
Extracellular Traps ◽  
Inflammatory Signals ◽  
Rapid Release ◽  
Specific Granules ◽  
Recognition Receptor

The long pentraxin (PTX) 3 is produced by macrophages and myeloid dendritic cells in response to Toll-like receptor agonists and represents a nonredundant component of humoral innate immunity against selected pathogens. We report that, unexpectedly, PTX3 is stored in specific granules and undergoes release in response to microbial recognition and inflammatory signals. Released PTX3 can partially localize in neutrophil extracellular traps formed by extruded DNA. Eosinophils and basophils do not contain preformed PTX3. PTX3-deficient neutrophils have defective microbial recognition and phagocytosis, and PTX3 is nonredundant for neutrophil-mediated resistance against Aspergillus fumigatus. Thus, neutrophils serve as a reservoir, ready for rapid release, of the long PTX3, a key component of humoral innate immunity with opsonic activity.

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 Neutrophil Extracellular Traps Sustain Inflammatory Signals in Ulcerative Colitis

2019 ◽  
Vol 13 (6) ◽  
pp. 772-784 ◽  
Author(s):  
Vincenzo Dinallo ◽  
Irene Marafini ◽  
Davide Di Fusco ◽  
Federica Laudisi ◽  
Eleonora Franzè ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Neutrophil Extracellular Traps ◽  
Extracellular Traps ◽  
Inflammatory Signals

scholarly journals Heparan Sulfate Modulates Neutrophil and Endothelial Function in Antibacterial Innate Immunity

2015 ◽  
Vol 83 (9) ◽  
pp. 3648-3656 ◽  
Author(s):  
Ding Xu ◽  
Joshua Olson ◽  
Jason N. Cole ◽  
Xander M. van Wijk ◽  
Volker Brinkmann ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Heparan Sulfate ◽  
Bactericidal Activity ◽  
Bacterial Pathogen ◽  
Systemic Infection ◽  
Neutrophil Extracellular Traps ◽  
Content Type ◽  
Extracellular Traps ◽  
The Central Nervous System ◽  
Group B

Recently, we showed that endothelial heparan sulfate facilitates entry of a bacterial pathogen into the central nervous system. Here, we show that normal bactericidal activity of neutrophils is influenced by the sulfation pattern of heparan sulfate. Inactivation of heparan sulfate uronyl 2-O-sulfotransferase (Hs2st) in neutrophils substantially reduced their bactericidal activity, and Hs2st deficiency rendered mice more susceptible to systemic infection with the pathogenic bacterium group BStreptococcus. Specifically, altered sulfation of heparan sulfate in mutant neutrophils affected formation of neutrophil extracellular traps while not influencing phagocytosis, production of reactive oxygen species, or secretion of granular proteases. Heparan sulfate proteoglycan(s) is present in neutrophil extracellular traps, modulates histone affinity, and modulates their microbial activity. Hs2st-deficient brain endothelial cells show enhanced binding to group BStreptococcusand are more susceptible to apoptosis, likely contributing to the observed increase in dissemination of group BStreptococcusinto the brain of Hs2st-deficient mice following intravenous challenge. Taken together, our data provide strong evidence that heparan sulfate from both neutrophils and the endothelium plays important roles in modulating innate immunity.

scholarly journals PSEUDOTUBERCULOSIS: PATHOGENETIC VALUE OF INNATE IMMUNITY CELLS

2017 ◽  
pp. 78-90
Author(s):  
L. M. Somova ◽  
N. G. Plekhova ◽  
E. I. Drobot ◽  
I. N. Lyapun
Keyword(s):  
Immune Deficiency ◽  
Innate Immunity ◽  
Neutrophil Extracellular Traps ◽  
Primary Immune Response ◽  
Protective Function ◽  
Extracellular Traps ◽  
Unique Pair ◽  
Causative Agents ◽  
Innate Immunity Cells ◽  
Far Eastern

Novel data on mechanisms of innate immunity during infections with pathogenic Yersiniae are summarized in the review, that was mostly determined by complex developments regarding a unique pair of genetically related causative agents Y. pseudotuberculosis/Y. pestis. Our previous studies have revealed a morphological substrate of relative granulocyte immune deficiency that determines characteristic pathomorphologic features of pseudotuberculosis. To date, evidence has been obtained, that pathogenic for human Yersinia predominately activate protective function of innate immunity cells that is an important strategy to avoid elimination and cause the disease for the bacteria. Neutrophils (PMNs) play a fundamental role in response to infection by pathogenic Yersiniae in primary immune response and limit of primary spread of bacteria that use several mechanisms of eradication ofbacteria, e.g.: phagocytosis, oxidative stress, secretory degranulation, formation of neutrophil extracellular traps, efferocytosis. Infected PMNs can act as an intermediate host for consequent non-inflammatory infection of macrophages. Further elaboration of questions relating to primary anti-infection protection during Yersinia infections gives a key to understanding of immune pathogenesis of epidemic pseudotuberculosis (far Eastern scarlet-like fever) and yersiniosis in general.

Neutrophil extracellular traps as a new paradigm in innate immunity: friend or foe?

2013 ◽  
Vol 63 (1) ◽  
pp. 165-197 ◽  
Author(s):  
Paul R. Cooper ◽  
Lisa J. Palmer ◽  
Iain L. C. Chapple
Keyword(s):  
Innate Immunity ◽  
Neutrophil Extracellular Traps ◽  
New Paradigm ◽  
Extracellular Traps

scholarly journals PAD4 is essential for antibacterial innate immunity mediated by neutrophil extracellular traps

2010 ◽  
Vol 207 (9) ◽  
pp. 1853-1862 ◽  
Author(s):  
Pingxin Li ◽  
Ming Li ◽  
Michael R. Lindberg ◽  
Mary J. Kennett ◽  
Na Xiong ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Bacterial Infection ◽  
Disease Model ◽  
Neutrophil Extracellular Traps ◽  
Chromatin Decondensation ◽  
Bacterial Killing ◽  
Infectious Disease Model ◽  
Extracellular Traps ◽  
Decondensed Chromatin

Neutrophils trap and kill bacteria by forming highly decondensed chromatin structures, termed neutrophil extracellular traps (NETs). We previously reported that histone hypercitrullination catalyzed by peptidylarginine deiminase 4 (PAD4) correlates with chromatin decondensation during NET formation. However, the role of PAD4 in NET-mediated bacterial trapping and killing has not been tested. Here, we use PAD4 knockout mice to show that PAD4 is essential for NET-mediated antibacterial function. Unlike PAD4+/+ neutrophils, PAD4−/− neutrophils cannot form NETs after stimulation with chemokines or incubation with bacteria, and are deficient in bacterial killing by NETs. In a mouse infectious disease model of necrotizing fasciitis, PAD4−/− mice are more susceptible to bacterial infection than PAD4+/+ mice due to a lack of NET formation. Moreover, we found that citrullination decreased the bacterial killing activity of histones and nucleosomes, which suggests that PAD4 mainly plays a role in chromatin decondensation to form NETs instead of increasing histone-mediated bacterial killing. Our results define a role for histone hypercitrullination in innate immunity during bacterial infection.

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