Evidence map›Paper›PMID 31134066›Full record

ReviewFrontiers in immunology2019

Glycans as Modulators for the Formation and Functional Properties of Neutrophil Extracellular Traps: Used by the Forces of Good and Evil.

Kim F Bornhöfft, Sebastian P Galuska

Abstract readReview
In one paragraph

Review in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed.

  1. Article
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  5. Influence of glycan structure on the colonization ofProceedings of the National Academy of Sciences of the United States of America · 2023
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  6. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Kim F BornhöfftInstitute of Reproductive Biology, Leibniz Institute for Farm Animal Biology, Dummerstorf, Germany.
Sebastian P GaluskaInstitute of Reproductive Biology, Leibniz Institute for Farm Animal Biology, Dummerstorf, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A very common mechanism to trap pathogens is the release of DNA. Like flies in a spider's web, pathogens are enclosed in a sticky chromatin meshwork. Interestingly, plants already use this mechanism to catch bacteria. In mammals, especially neutrophils release their DNA to prevent an invasion of bacteria. These neutrophil extracellular traps (NETs) are equipped with antimicrobial molecules, including, for instance, histones, antimicrobial peptides, lactoferrin, and neutrophil elastase. Thus, in a defined area, pathogens and toxic molecules are directly adjacent. However, several of these antimicrobial substances are also cytotoxic for endogenous cells. It is, therefore, not surprising that distinct control mechanisms exist to prevent an exaggerated NETosis. Nevertheless, despite these endogenous control instruments, an extraordinary NET release is characteristic for several pathologies. Consequently, NETs are a novel target for developing therapeutic strategies. In this review, we summarize the roles of glycans in the biology of NETs; on the one hand, we focus on the glycan-dependent strategies of endogenous cells to control NET formation or to inactivate its cytotoxic effects, and, on the other hand, the "sweet" tricks of pathogens to inhibit the release of NETs or to prevent NET-mediated killing mechanisms are examined. Understanding both, the forces of good and evil, allows the development of novel glycan-based approaches to combat the harmful side of NETs during distinct pathologies.

Indexed as

AnimalsExtracellular TrapsGlycosylationHumansNeutrophilsPolysaccharidesPolysaccharidesglycosaminoglycanshistonesNETosispolysialic acidSiglecs

Identifiers

PMID31134066
PMCPMC6514094

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.