Evidence map›Paper›PMID 28138158›Full record

Trial reportMolecular psychiatry2017

Selective increase of cerebrospinal fluid IL-6 during experimental systemic inflammation in humans: association with depressive symptoms.

H Engler, P Brendt, J Wischermann, A Wegner, R Röhling, T Schoemberg, U Meyer, R Gold, J Peters, S Benson and 1 more

Abstract readRandomized Controlled Trial
PubMed Publisher
In one paragraph

Trial report in Molecular psychiatry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
4.6field-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

61 citing papers in PubMed, 121 citations in OpenAlex.

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  9. Article
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  12. Antidepressant-like Effects ofPharmaceuticals (Basel, Switzerland) · 2024
    Article
  13. CD4Neurobiology of stress · 2024
    Article
  14. Metabolic Endotoxemia: From the Gut to Neurodegeneration.International journal of molecular sciences · 2024
    Review
  15. Biomarkers of stress resilience: A review.Neuroscience applied · 2024
    Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article

1 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

11 authors at 3 institutions in 2 countries.

H EnglerInstitute of Medical Psychology and Behavioral Immunobiology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
P BrendtClinic for Anesthesiology and Intensive Care Medicine, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
J WischermannClinic for Anesthesiology and Intensive Care Medicine, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
A WegnerDepartment of Orthopedic and Trauma Surgery, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
R RöhlingInstitute of Medical Psychology and Behavioral Immunobiology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
T SchoembergDepartment of Neurosurgery, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
U MeyerInstitute of Pharmacology and Toxicology, University of Zurich-Vetsuisse, Zurich, Switzerland.
R GoldDepartment of Neurology, St Josef-Hospital, Ruhr University, Bochum, Germany.
J PetersClinic for Anesthesiology and Intensive Care Medicine, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
S BensonInstitute of Medical Psychology and Behavioral Immunobiology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.ORCID 0000-0002-4487-4258
M SchedlowskiInstitute of Medical Psychology and Behavioral Immunobiology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
University of Duisburg-Essen · DESt. Josef-Hospital · DEUniversity of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Systemic inflammation is accompanied by profound behavioral and mood changes that resemble symptoms of depression. Findings in animals suggest that pro-inflammatory cytokines released by activated immune cells in the periphery evoke these behavioral symptoms by driving inflammatory changes in the brain. However, experimental data in humans are lacking. Here we demonstrate in healthy male volunteers (10 endotoxin treated, 8 placebo treated) that intravenous administration of low-dose endotoxin (0.8 ng/kg body weight), a prototypical pathogen-associated molecular pattern that activates the innate immune system, not only induces a significant increase in peripheral blood cytokine concentrations (that is, tumor necrosis factor-α, interleukin (IL)-6, IL-10) but also results, with some latency, in a robust and selective increase of IL-6 in the cerebrospinal fluid (CSF). Moreover, we found a strong association between the endotoxin-induced increase of IL-6 in the CSF and the severity of mood impairment, with larger increases in CSF IL-6 concentration followed by a greater deterioration in mood. Taken together, these findings suggest that the appearance of depressive symptoms in inflammatory conditions might be primarily linked to an increase in central IL-6 concentration, identifying IL-6 as a potential therapeutic target in mood disorders.

Indexed as

AdultCytokinesDepressionEndotoxinsHumansImmunity, InnateInflammationInterleukin-6MaleYoung AdultCytokinesEndotoxinsIL6 protein, humanInterleukin-6

Identifiers

PMID28138158
OpenAlexW2585572290

What OpenQuestion holds

Textmetadata
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.