
DOI . ORG {
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Title[redir]:
Modulation of neutrophil NETosis: interplay between infectious agents and underlying host physiology | Seminars in Immunopathology
Description:
The ability of neutrophils and other leucocyte members of the innate immune system to expel their DNA into the extracellular environment in a controlled manner in order to trap and kill pathogenic microorganisms lead to a paradigm shift in our understanding of host microbe interactions. Surprisingly, the neutrophil extracellular trap (NET) cast by neutrophils is very wide and extends to the entrapment of viruses as well as multicellular eukaryotic parasites. Not unexpectedly, it has emerged that pathogenic microorganisms can employ a wide array of strategies to avoid ensnarement, including expression of DNAse enzymes that destroy the lattice backbone of NETs. Alternatively, they may use molecular mimicry to avoid detection or trigger events leading to the expression of immune modulatory cytokines such as IL-10, which dampen the NETotic response of neutrophils. In addition, the host microenvironment may contribute to the innate immune response by the production of lectin-like molecules that bind to bacteria and promote their entrapment on NETs. An example of this is the production of surfactant protein D by the lung epithelium. In addition, pregnancy provides a different challenge, as the mother needs to mount an effective response against pathogens, without harming her unborn child. An examination of these decoy and host response mechanisms may open the path for new therapies to treat pathologies mediated by overt NETosis.
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Keywords {🔍}
google, scholar, article, pubmed, cas, neutrophil, nets, extracellular, neutrophils, immune, host, response, cells, innate, pmn, tuberculosis, netosis, traps, infections, human, infection, cell, hiv, antimicrobial, pathogens, bacterial, macrophages, system, cathelicidin, pmns, journal, dna, immunol, bacteria, blood, bacilli, pregnancy, immunity, shown, role, interaction, peptide, net, strategies, action, fig, viral, microorganisms, promote, elastase,
Topics {✒️}
gp120/cd-sign-primed dcs staphylococcus aureus-derived proteinases article download pdf potent immune-modulating cytokines multiple immune-modulatory functions bovis bacillus calmette-guérin time-lapse fluorescence microscopy asymptomatic felv-infected cats symptomatic felv-infected cats cytotoxic dna–protein complexes immune-modulating cytokine il-10 related subjects autoimmune small-vessel vasculitis chanchal sur chowdury underlying host physiology von willebrand factor cg/ne-loaded liposomes anti-hiv therapeutic strategies antimicrobial substances generated murine pmn response promote staphylokinase-dependent fibrinolysis wide-field fluorescence microscopy neutrophil extracellular traps potent immune response acute lung injury neutrophil extracellular trap host immune response opportunistic pathogen exploits malaria parasite promotes bacterial trapping dnase molecule sda1 innate immune response paul hasler privacy choices/manage cookies phagocyte extracellular traps staphylococcus aureus disease caspase-1-independent cell death environmental tobacco smoke human alpha-defensins immune modulatory cytokines plasmacytoid dendritic cells extracellular dna traps systemic lupus erythematosus immune–thrombotic response [59] effective immune response bactericidal granular proteins individual dna fibers infected lung tissue fetal growth restriction airway mucus formation
Questions {❓}
- Downmodulation of NETosis by HIV: paving the way for secondary infections?
- Feltcher ME et al (2010) Protein export systems of Mycobacterium tuberculosis: novel targets for drug development?
- Gupta A et al (2006) Occurrence of neutrophil extracellular DNA traps (NETs) in pre-eclampsia: a link with elevated levels of cell-free DNA?
- Lowe DM et al (2012) Neutrophils in tuberculosis: friend or foe?
- Malaria: a possible autoimmune component?
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headline:Modulation of neutrophil NETosis: interplay between infectious agents and underlying host physiology
description:The ability of neutrophils and other leucocyte members of the innate immune system to expel their DNA into the extracellular environment in a controlled manner in order to trap and kill pathogenic microorganisms lead to a paradigm shift in our understanding of host microbe interactions. Surprisingly, the neutrophil extracellular trap (NET) cast by neutrophils is very wide and extends to the entrapment of viruses as well as multicellular eukaryotic parasites. Not unexpectedly, it has emerged that pathogenic microorganisms can employ a wide array of strategies to avoid ensnarement, including expression of DNAse enzymes that destroy the lattice backbone of NETs. Alternatively, they may use molecular mimicry to avoid detection or trigger events leading to the expression of immune modulatory cytokines such as IL-10, which dampen the NETotic response of neutrophils. In addition, the host microenvironment may contribute to the innate immune response by the production of lectin-like molecules that bind to bacteria and promote their entrapment on NETs. An example of this is the production of surfactant protein D by the lung epithelium. In addition, pregnancy provides a different challenge, as the mother needs to mount an effective response against pathogens, without harming her unborn child. An examination of these decoy and host response mechanisms may open the path for new therapies to treat pathologies mediated by overt NETosis.
datePublished:2013-05-07T00:00:00Z
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description:The ability of neutrophils and other leucocyte members of the innate immune system to expel their DNA into the extracellular environment in a controlled manner in order to trap and kill pathogenic microorganisms lead to a paradigm shift in our understanding of host microbe interactions. Surprisingly, the neutrophil extracellular trap (NET) cast by neutrophils is very wide and extends to the entrapment of viruses as well as multicellular eukaryotic parasites. Not unexpectedly, it has emerged that pathogenic microorganisms can employ a wide array of strategies to avoid ensnarement, including expression of DNAse enzymes that destroy the lattice backbone of NETs. Alternatively, they may use molecular mimicry to avoid detection or trigger events leading to the expression of immune modulatory cytokines such as IL-10, which dampen the NETotic response of neutrophils. In addition, the host microenvironment may contribute to the innate immune response by the production of lectin-like molecules that bind to bacteria and promote their entrapment on NETs. An example of this is the production of surfactant protein D by the lung epithelium. In addition, pregnancy provides a different challenge, as the mother needs to mount an effective response against pathogens, without harming her unborn child. An examination of these decoy and host response mechanisms may open the path for new therapies to treat pathologies mediated by overt NETosis.
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