Evidence map›Paper›PMID 31906991›Full record

ArticleJournal of neuroinflammation2020

Toll-like receptor 4 agonist and antagonist lipopolysaccharides modify innate immune response in rat brain circumventricular organs.

Alejandra Vargas-Caraveo, Aline Sayd, Javier Robledo-Montaña, Javier R Caso, José L M Madrigal, Borja García-Bueno, Juan C Leza

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.1field-weighted citation impact, top 7% 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

28 citing papers in PubMed, 58 citations in OpenAlex.

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  8. Association of Cognitive Impairment and Peripheral Inflammation in Methamphetamine-dependent Patients: A Cross-sectional Study on Neuroinflammatory Markers TNF-α and IL-6.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2025
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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

7 authors at 1 institution in 2 countries.

Alejandra Vargas-CaraveoDepartamento de Farmacología y Toxicología, Facultad de Medicina, Universidad Complutense de Madrid (UCM); Centro de Investigación Biomédica en Red de Salud Mental (CIBERSAM); Instituto de Investigación Sanitaria Hospital 12 de Octubre (Imas12); Instituto Universitario de Investigación en Neuroquímica UCM, Avda. Complutense s/n, 28040, Madrid, Spain. a_vargas@correo.ler.uam.mx.
Aline SaydDepartamento de Farmacología y Toxicología, Facultad de Medicina, Universidad Complutense de Madrid (UCM); Centro de Investigación Biomédica en Red de Salud Mental (CIBERSAM); Instituto de Investigación Sanitaria Hospital 12 de Octubre (Imas12); Instituto Universitario de Investigación en Neuroquímica UCM, Avda. Complutense s/n, 28040, Madrid, Spain.
Javier Robledo-MontañaDepartamento de Farmacología y Toxicología, Facultad de Medicina, Universidad Complutense de Madrid (UCM); Centro de Investigación Biomédica en Red de Salud Mental (CIBERSAM); Instituto de Investigación Sanitaria Hospital 12 de Octubre (Imas12); Instituto Universitario de Investigación en Neuroquímica UCM, Avda. Complutense s/n, 28040, Madrid, Spain.
Javier R CasoDepartamento de Farmacología y Toxicología, Facultad de Medicina, Universidad Complutense de Madrid (UCM); Centro de Investigación Biomédica en Red de Salud Mental (CIBERSAM); Instituto de Investigación Sanitaria Hospital 12 de Octubre (Imas12); Instituto Universitario de Investigación en Neuroquímica UCM, Avda. Complutense s/n, 28040, Madrid, Spain.
José L M MadrigalDepartamento de Farmacología y Toxicología, Facultad de Medicina, Universidad Complutense de Madrid (UCM); Centro de Investigación Biomédica en Red de Salud Mental (CIBERSAM); Instituto de Investigación Sanitaria Hospital 12 de Octubre (Imas12); Instituto Universitario de Investigación en Neuroquímica UCM, Avda. Complutense s/n, 28040, Madrid, Spain.
Borja García-BuenoDepartamento de Farmacología y Toxicología, Facultad de Medicina, Universidad Complutense de Madrid (UCM); Centro de Investigación Biomédica en Red de Salud Mental (CIBERSAM); Instituto de Investigación Sanitaria Hospital 12 de Octubre (Imas12); Instituto Universitario de Investigación en Neuroquímica UCM, Avda. Complutense s/n, 28040, Madrid, Spain. bgbueno@med.ucm.es.ORCID http://orcid.org/0000-0001-7320-1530
Juan C LezaDepartamento de Farmacología y Toxicología, Facultad de Medicina, Universidad Complutense de Madrid (UCM); Centro de Investigación Biomédica en Red de Salud Mental (CIBERSAM); Instituto de Investigación Sanitaria Hospital 12 de Octubre (Imas12); Instituto Universitario de Investigación en Neuroquímica UCM, Avda. Complutense s/n, 28040, Madrid, Spain.
Universidad Complutense de Madrid · ES

Funding

Ministerio de Economía, Industria y Competitividad, Gobierno de España SAF2016-75500-RMinisterio de Economía, Industria y Competitividad, Gobierno de España SAF2017-85888-R
6 · The paper itself

Abstract

backgroundThe circumventricular organs (CVOs) are blood-brain-barrier missing structures whose activation through lipopolysaccharide (LPS) is a starting point for TLR-driven (Toll-like receptors) neuroinflammation. The aim of this study was to evaluate in the CVO area postrema (AP), subfornical organ (SFO), and median eminence (ME), the inflammatory response to two TLR4 agonists: LPS from Escherichia coli (EC-LPS), the strongest endotoxin molecule described, and LPS from Porphyromonas gingivalis (PG-LPS), a pathogenic bacteria present in the periodontium related to neuroinflammation in neurodegenerative/psychiatric diseases. The response to LPS from the cyanobacteria Rhodobacter sphaeroides (RS-LPS), a TLR4 antagonist with an interesting anti-inflammatory potential, was also assessed.

methodsLPSs were intraperitoneally administered to Wistar rats and, as indicatives of neuroinflammation in CVOs, the cellular localization of the nuclear factor NF-κB was studied by immunofluorescence, and microglia morphology was quantified by fractal and skeleton analysis.

resultsData showed that EC-LPS increased NF-κB nuclear translocation in the three CVOs studied and PG-LPS only induced NF-κB nuclear translocation in the ME. RS-LPS showed no difference in NF-κB nuclear translocation compared to control. Microglia in the three CVOs showed an ameboid-shape after EC-LPS exposure, whereas PG-LPS only elicited a mild tendency to induce an ameboid shape. On the other hand, RS-LPS produced a markedly elongated morphology described as "rod" microglia in the three CVOs.

conclusionsIn conclusion, at the doses tested, EC-LPS induces a stronger neuroinflammatory response than PG-LPS in CVOs, which might be related to their different potency as TLR4 agonists. The non-reduction of basal NF-κB activation and induction of rod microglia by RS-LPS, a cell morphology only present in severe brain injury and infections, suggests that this molecule must be carefully studied before being proposed as an anti-inflammatory treatment for neuroinflammation related to neurodegenerative/psychiatric diseases.

Indexed as

AnimalsBrainCircumventricular OrgansImmunity, InnateLipopolysaccharidesMaleNF-kappa BRatsRats, WistarToll-Like Receptor 4LipopolysaccharidesNF-kappa BTlr4 protein, ratToll-Like Receptor 4Bacterial infectionBlood-brain interfacesImmunofluorescenceInnate immunityMicroglia

Identifiers

PMID31906991
PMCPMC6945636
OpenAlexW3001189769

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.