netosis and nadph oxidase: at the intersection of host defense, inflammation, and injury

Clicks: 218
ID: 238621
2013
Free PDF
Article Quality & Performance Metrics
Overall Quality
Not rated
Combines reader engagement with the AI quality analysis. This article has not been analysed, so there is no overall score — reader engagement is measured and shown alongside.
AI Quality Assessment
Not analyzed
Readership in this journal
Popular

Ranked #552 of 644 articles by views in sudebno-meditsinskaia ekspertiza

Most read Least read

Bar heights use a square-root scale. Only the 120 most-read articles are drawn; the journal has 644 in total.

Mint this article as an NFT
Not yet minted

Create a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.

5 SUSD one-off · no wallet required
Sign in to mint
Abstract
Neutrophils are armed with both oxidant-dependent and –independent pathways for killing pathogens. Activation of the phagocyte NADPH oxidase constitutes an emergency response to infectious threat and results in the generation of antimicrobial reactive oxidants. In addition, NADPH oxidase activation in neutrophils is linked to activation of granular proteases and generation of neutrophil extracellular traps (NETs). NETosis involves the release of nuclear and granular components that can target extracellular pathogens. NETosis is activated during microbial threat and in certain conditions mimicking sepsis, and can result in both augmented host defense and inflammatory injury. In contrast, apoptosis, the physiological form of neutrophil death, not only leads to non-inflammatory cell death but also contributes to alleviate inflammation. Although there are significant gaps in knowledge regarding the specific contribution of NETs to host defense, we speculate that the coordinated activation of NADPH oxidase and NETosis maximizes microbial killing. Work in engineered mice and limited patient experience point to varying susceptibility of bacterial and fungal pathogens to NADPH oxidase versus NET constituents. Since reactive oxidants and NET constituents can injure host tissue, it is important that these pathways be tightly regulated. Recent work supports a role for NETosis in both acute lung injury and in autoimmunity. Knowledge gained about mechanisms that modulate NETosis may lead to novel therapeutic approaches to limit inflammation-associated injury.
Reference Key
ealmyroudis2013frontiersnetosis Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors ;Nikolaos eAlmyroudis;Nikolaos eAlmyroudis;Melissa eGrimm;Bruce eDavidson;Marc eRohm;Constantin eUrban;Brahm eSegal;Brahm eSegal
Journal sudebno-meditsinskaia ekspertiza
Year 2013
DOI
10.3389/fimmu.2013.00045
URL
http://journal.frontiersin.org/Journal/10.3389/fimmu.2013.00045/full
Keywords
host defense inflammation injury allergy

Citations

No citations found. To add a citation, contact the admin at info@scimatic.org

Comments

No comments yet. Be the first to comment on this article.