Evidence map›Paper›PMID 30319656›Full record

ArticleFrontiers in immunology2018

Exposure of Monocytic Cells to Lipopolysaccharide Induces Coordinated Endotoxin Tolerance, Mitochondrial Biogenesis, Mitophagy, and Antioxidant Defenses.

John D Widdrington, Aurora Gomez-Duran, Angela Pyle, Marie-Helene Ruchaud-Sparagano, Jonathan Scott, Simon V Baudouin, Anthony J Rostron, Penny E Lovat, Patrick F Chinnery, A John Simpson

Open access · goldAbstract read
In one paragraph

Article 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 45 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 11% 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

45 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.

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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

10 authors at 4 institutions in 1 country.

John D WiddringtonInstitute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, United Kingdom.
Aurora Gomez-DuranInstitute of Genetic Medicine, Newcastle University, Newcastle upon Tyne, United Kingdom.
Angela PyleInstitute of Genetic Medicine, Newcastle University, Newcastle upon Tyne, United Kingdom.
Marie-Helene Ruchaud-SparaganoInstitute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, United Kingdom.
Jonathan ScottInstitute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, United Kingdom.
Simon V BaudouinDepartment of Anaesthesia, Royal Victoria Infirmary, Newcastle upon Tyne, United Kingdom.
Anthony J RostronInstitute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, United Kingdom.
Penny E LovatInstitute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, United Kingdom.
Patrick F ChinneryInstitute of Genetic Medicine, Newcastle University, Newcastle upon Tyne, United Kingdom.
A John SimpsonInstitute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, United Kingdom.
Newcastle University · GBMRC Mitochondrial Biology Unit · GBRoyal Victoria Infirmary · GBUniversity of Cambridge · GB

Funding

Medical Research Council MC_UP_1501/2Medical Research Council MR/N02995X/1Wellcome Trust
6 · The paper itself

Abstract

In order to limit the adverse effects of excessive inflammation, anti-inflammatory responses are stimulated at an early stage of an infection, but during sepsis these can lead to deactivation of immune cells including monocytes. In addition, there is emerging evidence that the up-regulation of mitochondrial quality control mechanisms, including mitochondrial biogenesis and mitophagy, is important during the recovery from sepsis and inflammation. We aimed to describe the relationship between the compensatory immune and mitochondrial responses that are triggered following exposure to an inflammatory stimulus in human monocytic cells. Incubation with lipopolysaccharide resulted in a change in the immune phenotype of THP-1 cells consistent with the induction of endotoxin tolerance, similar to that seen in deactivated septic monocytes. After exposure to LPS there was also early evidence of oxidative stress, which resolved in association with the induction of antioxidant defenses and the stimulation of mitochondrial degradation through mitophagy. This was compensated by a parallel up-regulation of mitochondrial biogenesis that resulted in an overall increase in mitochondrial respiratory activity. These observations improve our understanding of the normal homeostatic responses that limit the adverse cellular effects of unregulated inflammation, and which may become ineffective when an infection causes sepsis.

Indexed as

Organelle BiogenesisEndotoxinsHumansImmune ToleranceLipopolysaccharidesMitochondriaMitophagyMonocytesOxidative StressTHP-1 CellsEndotoxinsLipopolysaccharidesantioxidantsendotoxin toleranceinflammationmitochondriamitochondrial biogenesismitophagymtDNA

Identifiers

PMID30319656
PMCPMC6170658
OpenAlexW2893278511

What OpenQuestion holds

Textmetadata
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.