Evidence map›Paper›PMID 31781091›Full record

ArticleFrontiers in immunology2019

Memory-Like Inflammatory Responses of Microglia to Rising Doses of LPS: Key Role of PI3Kγ.

Trim Lajqi, Guang-Ping Lang, Fabienne Haas, David L Williams, Hannes Hudalla, Michael Bauer, Marco Groth, Reinhard Wetzker, Reinhard Bauer

Open access · goldAbstract read
In one paragraph

Article 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 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

63 citing papers in PubMed, 98 citations in OpenAlex.

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  13. Structure matters: commensalFrontiers in cellular neuroscience · 2026
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3 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

9 authors at 4 institutions in 2 countries.

Trim LajqiInstitute of Molecular Cell Biology, Jena University Hospital, Jena, Germany.
Guang-Ping LangInstitute of Molecular Cell Biology, Jena University Hospital, Jena, Germany.
Fabienne HaasInstitute of Molecular Cell Biology, Jena University Hospital, Jena, Germany.
David L WilliamsDepartment of Surgery and Center of Excellence in Inflammation, Infectious Disease and Immunity, Quillen College of Medicine, East Tennessee State University, Johnson City, TN, United States.
Hannes HudallaDepartment of Neonatology, Heidelberg University Children's Hospital, Heidelberg, Germany.
Michael BauerDepartment of Anesthesiology and Intensive Care Medicine, Jena University Hospital, Jena, Germany.
Marco GrothLeibniz Institute on Aging-Fritz Lipmann Institute, CF DNA Sequencing, Jena, Germany.
Reinhard WetzkerDepartment of Anesthesiology and Intensive Care Medicine, Jena University Hospital, Jena, Germany.
Reinhard BauerInstitute of Molecular Cell Biology, Jena University Hospital, Jena, Germany.
Jena University Hospital · DEEast Tennessee State University · USHeidelberg University · DELeibniz Institute on Aging - Fritz Lipmann Institute (FLI) · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Trained immunity and immune tolerance have been identified as long-term response patterns of the innate immune system. The causes of these opposing reactions remain elusive. Here, we report about differential inflammatory responses of microglial cells derived from neonatal mouse brain to increasing doses of the endotoxin LPS. Prolonged priming with ultra-low LPS doses provokes trained immunity, i.e., increased production of pro-inflammatory mediators in comparison to the unprimed control. In contrast, priming with high doses of LPS induces immune tolerance, implying decreased production of inflammatory mediators and pronounced release of anti-inflammatory cytokines. Investigation of the signaling processes and cell functions involved in these memory-like immune responses reveals the essential role of phosphoinositide 3-kinase γ (PI3Kγ), one of the phosphoinositide 3-kinase species highly expressed in innate immune cells. Together, our data suggest profound influence of preceding contacts with pathogens on the immune response of microglia. The impact of these interactions-trained immunity or immune tolerance-appears to be shaped by pathogen dose.

Indexed as

AnimalsAnimals, NewbornBrainCells, CulturedClass Ib Phosphatidylinositol 3-KinaseCytokinesImmune ToleranceImmunity, InnateImmunologic MemoryInflammation MediatorsLipopolysaccharidesMiceMice, Inbred C57BLMice, KnockoutMicrogliaClass Ib Phosphatidylinositol 3-KinaseCytokinesInflammation MediatorsLipopolysaccharidesPik3cg protein, mouseLPSmicrogliaphagocytosisPI3Kγtolerancetrainingβ-glucan

Identifiers

PMID31781091
PMCPMC6856213
OpenAlexW2988557783

What OpenQuestion holds

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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.