Evidence map›Paper›PMID 33028343›Full record

ArticleJournal of neuroinflammation2020

Impact of ambient temperature on inflammation-induced encephalopathy in endotoxemic mice-role of phosphoinositide 3-kinase gamma.

Guang-Ping Lang, Bernadin Ndongson-Dongmo, Trim Lajqi, Michael Brodhun, Yingying Han, Reinhard Wetzker, Martin G Frasch, Reinhard Bauer

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.7field-weighted citation impact, top 28% 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

11 citing papers in PubMed, 15 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

8 authors at 7 institutions in 4 countries.

Guang-Ping LangInstitute of Molecular Cell Biology, Jena University Hospital, Friedrich Schiller University, Hans-Knöll-Straße 2, D-07745, Jena, Germany.
Bernadin Ndongson-DongmoInstitute of Molecular Cell Biology, Jena University Hospital, Friedrich Schiller University, Hans-Knöll-Straße 2, D-07745, Jena, Germany.
Trim LajqiInstitute of Molecular Cell Biology, Jena University Hospital, Friedrich Schiller University, Hans-Knöll-Straße 2, D-07745, Jena, Germany.
Michael BrodhunDepartment of Pathology, Helios-Klinikum Erfurt, Erfurt, Germany.
Yingying HanInstitute of Biochemistry I, Faculty of Medicine, Goethe-University Frankfurt, 60590, Frankfurt, Germany.
Reinhard WetzkerDepartment of Anesthesiology and Intensive Care Medicine, Jena University Hospital, Friedrich Schiller University, Jena, Germany.
Martin G FraschUniversity of Washington School of Medicine, Seattle, WA, USA.
Reinhard BauerInstitute of Molecular Cell Biology, Jena University Hospital, Friedrich Schiller University, Hans-Knöll-Straße 2, D-07745, Jena, Germany. Reinhard.Bauer@med.uni-jena.de.ORCID http://orcid.org/0000-0002-4294-3758
Jena University Hospital · DEGoethe University Frankfurt · DEHeidelberg University · DEHelios Klinikum Erfurt · DEOslo University Hospital · NOUniversity of Washington · USZunyi Medical University · CN

Funding

Mechanisms of Brain Dysmorphology in MN1 C-Terminal Truncation Syndrome, a Novel Intellectual Developmental Disability Disorder P50HD103524 · NICHD · UNIVERSITY OF WASHINGTON · PI Sandra E Juul · 2020 to 2026
$9.9M
Deutsche Forschungsgemeinschaft RTG 1715European Union Seventh Framework Programme (FP7-PEOPLE-2013-COFUND 609020-Scientia FellowsNICHD NIH HHS P50 HD103524
6 · The paper itself

Abstract

backgroundSepsis-associated encephalopathy (SAE) is an early and frequent event of infection-induced systemic inflammatory response syndrome. Phosphoinositide 3-kinase γ (PI3Kγ) is linked to neuroinflammation and inflammation-related microglial activity. In homeotherms, variations in ambient temperature (T

methodsExperiments were performed in wild-type, PI3Kγ knockout, and PI3Kγ kinase-dead mice, which were kept at neutral (30 ± 0.5 °C) or moderately lowered (26 ± 0.5 °C) T

resultsWe show that a moderate reduction of ambient temperature triggers enhanced hypothermia of mice undergoing LPS-induced systemic inflammation by aggravated SAE. PI3Kγ deficiency enhances blood-brain barrier injury and upregulation of matrix metalloproteinases (MMPs) as well as an impaired microglial phagocytic activity.

conclusionsThermoregulatory adaptation in response to ambient temperatures below the thermoneutral range exacerbates LPS-induced blood-brain barrier injury and neuroinflammation. PI3Kγ serves a protective role in suppressing release of MMPs, maintaining microglial motility and reinforcing phagocytosis leading to improved brain tissue integrity. Thus, preclinical research targeting severe brain inflammation responses is seriously biased when basic physiological prerequisites of mammal species such as preferred ambient temperature are ignored.

Indexed as

AnimalsAnimals, NewbornBlood-Brain BarrierBody TemperatureBody Temperature RegulationCells, CulturedClass Ib Phosphatidylinositol 3-KinaseFemaleLipopolysaccharidesMaleMiceMice, Inbred C57BLMice, KnockoutSepsis-Associated EncephalopathyClass Ib Phosphatidylinositol 3-KinaseLipopolysaccharidesPik3cg protein, mouseAmbient temperatureBlood–brain barrierMatrix metalloproteinasesMicrogliaMigrationNeuroinflammationPhagocytosisPhosphoinositide 3-kinase γ

Identifiers

PMID33028343
PMCPMC7541275
OpenAlexW3092470931

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.