Evidence map›Paper›PMID 29880000›Full record

ArticleJournal of neuroinflammation2018

Activin A increases phagocytosis of Escherichia coli K1 by primary murine microglial cells activated by toll-like receptor agonists.

Catharina Diesselberg, Sandra Ribes, Jana Seele, Annika Kaufmann, Sandra Redlich, Stephanie Bunkowski, Uwe-Karsten Hanisch, Uwe Michel, Roland Nau, Sandra Schütze

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.8field-weighted citation impact, top 27% 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

13 citing papers in PubMed, 20 citations in OpenAlex.

  1. Doxycycline-Induced Apoptosis inInfection and drug resistance · 2025
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  11. Effects ofPathogens (Basel, Switzerland) · 2019
    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.

Catharina DiesselbergInstitute of Neuropathology, University Medical Center Göttingen, Robert-Koch-Str. 40, 37075, Göttingen, Germany.
Sandra RibesInstitute of Neuropathology, University Medical Center Göttingen, Robert-Koch-Str. 40, 37075, Göttingen, Germany.
Jana SeeleInstitute of Neuropathology, University Medical Center Göttingen, Robert-Koch-Str. 40, 37075, Göttingen, Germany.
Annika KaufmannInstitute of Neuropathology, University Medical Center Göttingen, Robert-Koch-Str. 40, 37075, Göttingen, Germany.
Sandra RedlichInstitute of Neuropathology, University Medical Center Göttingen, Robert-Koch-Str. 40, 37075, Göttingen, Germany.
Stephanie BunkowskiInstitute of Neuropathology, University Medical Center Göttingen, Robert-Koch-Str. 40, 37075, Göttingen, Germany.
Uwe-Karsten HanischInstitute of Neuropathology, University Medical Center Göttingen, Robert-Koch-Str. 40, 37075, Göttingen, Germany.
Uwe MichelDepartment of Neurology, University Medical Center Göttingen, Robert-Koch-Str. 40, 37075, Göttingen, Germany.
Roland NauInstitute of Neuropathology, University Medical Center Göttingen, Robert-Koch-Str. 40, 37075, Göttingen, Germany.
Sandra SchützeInstitute of Neuropathology, University Medical Center Göttingen, Robert-Koch-Str. 40, 37075, Göttingen, Germany. sandra.schuetze@medizin.uni-goettingen.de.ORCID http://orcid.org/0000-0002-3692-2627
Universitätsmedizin Göttingen · DE

Funding

Robert Bosch Stiftung Forschungskolleg Geriatrie
6 · The paper itself

Abstract

backgroundBacterial meningitis is associated with high mortality and long-term neurological sequelae. Increasing the phagocytic activity of microglia could improve the resistance of the CNS against infections. We studied the influence of activin A, a member of the TGF-β family with known immunoregulatory and neuroprotective effects, on the functions of microglial cells in vitro.

methodsPrimary murine microglial cells were treated with activin A (0.13 ng/ml-13 μg/ml) alone or in combination with agonists of TLR2, 4, and 9. Phagocytosis of Escherichia coli K1 as well as release of TNF-α, IL-6, CXCL1, and NO was assessed.

resultsActivin A dose-dependently enhanced the phagocytosis of Escherichia coli K1 by microglial cells activated by agonists of TLR2, 4, and 9 without further increasing NO and proinflammatory cytokine release. Cell viability of microglial cells was not affected by activin A.

conclusionsPriming of microglial cells with activin A could increase the elimination of bacteria in bacterial CNS infections. This preventive strategy could improve the resistance of the brain to infections, particularly in elderly and immunocompromised patients.

Indexed as

ActivinsAnimalsAnimals, NewbornBrainCells, CulturedCytokinesDose-Response Relationship, DrugEscherichia coliHumansInfant, NewbornLipopolysaccharidesMiceMice, Inbred C57BLMicrogliaNitric OxidePhagocytosisactivin AActivinsCytokinesGriffonia simplicifolia lectinsLipopolysaccharidesNitric OxidePlant LectinsToll-Like ReceptorsActivinBacterial meningitisCNS infectionE. coliInnate immune systemNitric oxidePhagocytosisProinflammatory cytokinesTLR

Identifiers

PMID29880000
PMCPMC5992782
OpenAlexW2806501052

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.