Evidence map›Paper›PMID 29868038›Full record

ArticleFrontiers in immunology2018

Pro-Inflammatory Th1 and Th17 Cells Are Suppressed During Human Experimental Endotoxemia Whereas Anti-Inflammatory IL-10 Producing T-Cells Are Unaffected.

Alexandra Brinkhoff, Annette Sieberichs, Harald Engler, Sebastian Dolff, Sven Benson, Johannes Korth, Manfred Schedlowski, Andreas Kribben, Oliver Witzke, Benjamin Wilde

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 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

23 citing papers in PubMed, 33 citations in OpenAlex.

  1. Trial
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  8. Cholesterol Transport Dysfunction and Its Involvement in Atherogenesis.International journal of molecular sciences · 2022
    Review
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  13. Storm of Cardiovascular Markers After LPS Administration in Human Volunteers.Journal of cardiovascular translational research · 2021
    Article
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  15. Article
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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 1 institution in 1 country.

Alexandra BrinkhoffDepartment of Nephrology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Annette SieberichsDepartment of Nephrology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Harald EnglerInstitute of Medical Psychology and Behavioral Immunobiology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Sebastian DolffDepartment of Infectious Diseases, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Sven BensonInstitute of Medical Psychology and Behavioral Immunobiology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Johannes KorthDepartment of Nephrology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Manfred SchedlowskiInstitute of Medical Psychology and Behavioral Immunobiology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Andreas KribbenDepartment of Nephrology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Oliver WitzkeDepartment of Infectious Diseases, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Benjamin WildeDepartment of Nephrology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
University of Duisburg-Essen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objective: Sepsis is one of the leading causes of the deaths in hospitals. During sepsis, patients are exposed to endotoxemia, which may contribute to the dysregulation of the immune system frequently observed in sepsis. This dysregulation leads to impaired pro-inflammatory responses and may increase the risk for secondary infections in sepsis. The experimental human endotoxemia model is widely used as a model system to study the acute effects of endotoxemia. Under physiological circumstances, the immune system is tightly regulated. Effector T-cells exert pro-inflammatory function and are restrained by regulatory T-cells (Tregs), which modulate pro-inflammatory effector responses. Endotoxemia may induce inadequate Treg activity or render effector T-cells dysfunctional. It was the aim of the study to investigate effector T-cell and Treg responses in an experimental human endotoxemia model. Methods: In a cross-over designed placebo-controlled study, 20 healthy male volunteers received an intravenous injection of either lipopolysaccharide (LPS) (0.8 ng/kg body weight) or a placebo (saline 0.9%). CD3 Results: Circulating neutrophils were significantly increased 2 h after LPS injection ( Conclusion: Effector THs fail to produce pro-inflammatory Th1-/Th17-associated cytokines after LPS challenge. In contrast, IL-10 production by Treg is not affected. Thus, endotoxemia-induced suppression of pro-inflammatory THs might be considered as a contributing factor to immunoparalysis in sepsis.

Indexed as

AdolescentAdultBiomarkersCross-Over StudiesCytokinesEndotoxemiaHealthy VolunteersHumansImmunophenotypingInflammation MediatorsInterleukin-10Leukocyte CountLipopolysaccharidesMaleTh17 CellsTh1 CellsBiomarkersCytokinesIL10 protein, humanInflammation MediatorsInterleukin-10LipopolysaccharidesendotoxemiaIFNγIL-10IL-17Asystemic inflammationT-cellsTreg

Identifiers

PMID29868038
PMCPMC5968108
OpenAlexW2799324172

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.