Evidence map›Paper›PMID 29321478›Full record

ArticleScientific reports2018

Reprogramming of pro-inflammatory human macrophages to an anti-inflammatory phenotype by bile acids.

Marianne Wammers, Anna-Kathrin Schupp, Johannes G Bode, Christian Ehlting, Stephanie Wolf, René Deenen, Karl Köhrer, Dieter Häussinger, Dirk Graf

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
3.5field-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

49 citing papers in PubMed, 93 citations in OpenAlex.

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  4. Short-chain Fatty Acids and Bile Acids Signaling in Chronic Hepatitis B.Journal of clinical and translational hepatology · 2026
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Marianne WammersDepartment of Gastroenterology, Hepatology and Infectious Diseases, Heinrich-Heine-University Duesseldorf, Duesseldorf, Germany.
Anna-Kathrin SchuppDepartment of Gastroenterology, Hepatology and Infectious Diseases, Heinrich-Heine-University Duesseldorf, Duesseldorf, Germany.
Johannes G BodeDepartment of Gastroenterology, Hepatology and Infectious Diseases, Heinrich-Heine-University Duesseldorf, Duesseldorf, Germany.
Christian EhltingDepartment of Gastroenterology, Hepatology and Infectious Diseases, Heinrich-Heine-University Duesseldorf, Duesseldorf, Germany.
Stephanie WolfDepartment of Gastroenterology, Hepatology and Infectious Diseases, Heinrich-Heine-University Duesseldorf, Duesseldorf, Germany.
René DeenenBiological and Medical Research Centre (BMFZ), Cluster of Excellence on Plant Sciences (CEPLAS), Heinrich-Heine-University Duesseldorf, Duesseldorf, Germany.
Karl KöhrerBiological and Medical Research Centre (BMFZ), Cluster of Excellence on Plant Sciences (CEPLAS), Heinrich-Heine-University Duesseldorf, Duesseldorf, Germany.
Dieter HäussingerDepartment of Gastroenterology, Hepatology and Infectious Diseases, Heinrich-Heine-University Duesseldorf, Duesseldorf, Germany.
Dirk GrafDepartment of Gastroenterology, Hepatology and Infectious Diseases, Heinrich-Heine-University Duesseldorf, Duesseldorf, Germany. Dirk.Graf@med.uni-duesseldorf.de.
Heinrich Heine University Düsseldorf · DECluster of Excellence on Plant Sciences · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cholestasis is caused by autoimmune reactions, drug-induced hepatotoxicity, viral infections of the liver and the obstruction of bile ducts by tumours or gallstones. Cholestatic conditions are associated with impaired innate and adaptive immunity, including alterations of the cellular functions of monocytes, macrophages, NK cells and T-cells. Bile acids act as signalling molecules, affecting lipopolysaccharide (LPS)-induced cytokine expression in primary human macrophages. The present manuscript investigates the impact of bile acids, such as taurolithocholic acid (TLC), on the transcriptome of human macrophages in the presence or absence of LPS. While TLC itself has almost no effect on gene expression under control conditions, this compound modulates the expression of 202 out of 865 transcripts in the presence of LPS. Interestingly, pathway analysis revealed that TLC specifically supressed the expression of genes involved in mediating pro-inflammatory effects, phagocytosis, interactions with pathogens and autophagy as well as the recruitment of immune cells, such as NK cells, neutrophils and T cells. These data indicate a broad influence of bile acids on inflammatory responses and immune functions in macrophages. These findings may contribute to the clinical observation that patients with cholestasis present a lack of response to bacterial or viral infections.

Indexed as

Cellular ReprogrammingPhenotypeBile Acids and SaltsBiomarkersChemotaxisCytokinesGene Expression ProfilingGene Expression RegulationHumansInflammation MediatorsKiller Cells, NaturalLipopolysaccharidesMacrophage ActivationMacrophagesTranscriptomeBile Acids and SaltsBiomarkersCytokinesInflammation MediatorsLipopolysaccharides

Identifiers

PMID29321478
PMCPMC5762890
OpenAlexW2781867702

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.