Evidence map›Paper›PMID 30515175›Full record

ReviewFrontiers in immunology2018

Regulation of Endotoxin Tolerance and Compensatory Anti-inflammatory Response Syndrome by Non-coding RNAs.

Eleni Vergadi, Katerina Vaporidi, Christos Tsatsanis

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
3.8field-weighted citation impact, top 5% of its field
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

65 citing papers in PubMed, 121 citations in OpenAlex.

  1. Article
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  3. Review
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  11. Review
  12. Macrophage variants in laboratory research: most are well done, but some are RAW.Frontiers in cellular and infection microbiology · 2024
    Review
  13. Review
  14. Article
  15. Article
  16. Less Severe Polymicrobial Sepsis in ConditionalInternational journal of molecular sciences · 2023
    Article
  17. Less Severe Lipopolysaccharide-Induced Inflammation in ConditionalInternational journal of molecular sciences · 2023
    Article
  18. Article
  19. Article
  20. The Regulatory Roles ofInternational journal of molecular sciences · 2023
    Article

5 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Eleni VergadiDepartment of Paediatrics, Medical School, University of Crete, Heraklion, Greece.
Katerina VaporidiDepartment of Intensive Care Medicine, Medical School, University of Crete, Heraklion, Greece.
Christos TsatsanisDepartment of Clinical Chemistry, Medical School, University of Crete, Heraklion, Greece.
University of Crete · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The onset and the termination of innate immune response must be tightly regulated to maintain homeostasis and prevent excessive inflammation, which can be detrimental to the organism, particularly in the context of sepsis. Endotoxin tolerance and compensatory anti-inflammatory response syndrome (CARS) describe a state of hypo-responsiveness characterized by reduced capacity of myeloid cells to respond to inflammatory stimuli, particularly those initiated by bacterial lipopolysaccharide (LPS). To achieve endotoxin tolerance, extensive reprogramming otherwise termed as "innate immune training", is required that leads to both modifications of the intracellular components of TLR signaling and also to alterations in extracellular soluble mediators. Non-coding RNAs (ncRNAs) have been recognized as critical regulators of TLR signaling. Specifically, several microRNAs (miR-146, miR-125b, miR-98, miR-579, miR-132, let-7e and others) are induced upon TLR activation and reciprocally promote endotoxin tolerance and/or cross tolerance. Many other miRNAs have been also shown to negatively regulate TLR signaling. The long non-coding (lnc)RNAs (Mirt2, THRIL, MALAT1, lincRNA-21 and others) are also altered upon TLR activation and negatively regulate TLR signaling. Furthermore, the promotion or termination of myeloid cell tolerance is not only regulated by intracellular mediators but is also affected by other TLR-independent soluble signals that often achieve their effect via modulation of intracellular ncRNAs. In this article, we review recent evidence on the role of different ncRNAs in the context of innate immune cell tolerance and trained immunity, and evaluate their impact on immune system homeostasis.

Indexed as

Immune ToleranceImmunity, InnateAnimalsEndotoxinsHumansMicroRNAsRNA, Long NoncodingSystemic Inflammatory Response SyndromeToll-Like ReceptorsEndotoxinsMicroRNAsRNA, Long NoncodingToll-Like Receptorsendotoxin toleranceimmune suppressionlncRNAsmicroRNAsnon-coding RNAssepsissoluble mediators

Identifiers

PMID30515175
PMCPMC6255943
OpenAlexW2901973893

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.