Evidence map›Paper›PMID 24603356›Full record

ArticleBrain, behavior, and immunity2014

Interleukin 18 activates MAPKs and STAT3 but not NF-κB in hippocampal HT-22 cells.

Silvia Alboni, Claudia Montanari, Cristina Benatti, Manuel Sanchez-Alavez, Giovanna Rigillo, Joan M C Blom, Nicoletta Brunello, Bruno Conti, M Carmine Pariante, Fabio Tascedda

Open access · greenAbstract read
In one paragraph

Article in Brain, behavior, and immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

20 citing papers in PubMed, 46 citations in OpenAlex.

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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 3 institutions in 3 countries.

Silvia AlboniDepartment of Life Sciences, University of Modena and Reggio Emilia, Modena, Italy. Electronic address: silvia.alboni@unimore.it.
Claudia MontanariDepartment of Life Sciences, University of Modena and Reggio Emilia, Modena, Italy.
Cristina BenattiDepartment of Life Sciences, University of Modena and Reggio Emilia, Modena, Italy.
Manuel Sanchez-AlavezMolecular and Integrative Neurosciences Department, The Scripps Research Institute, La Jolla, CA 92037, United States.
Giovanna RigilloDepartment of Medical and Surgical Sciences for Children and Adults, University of Modena and Reggio Emilia, Modena, Italy.
Joan M C BlomDepartment of Medical and Surgical Sciences for Children and Adults, University of Modena and Reggio Emilia, Modena, Italy.
Nicoletta BrunelloDepartment of Life Sciences, University of Modena and Reggio Emilia, Modena, Italy.
Bruno ContiMolecular and Integrative Neurosciences Department, The Scripps Research Institute, La Jolla, CA 92037, United States.
M Carmine ParianteDepartment of Psychological Medicine, Institute of Psychiatry, Kings College London, London, UK.
Fabio TasceddaDepartment of Life Sciences, University of Modena and Reggio Emilia, Modena, Italy.
University of Modena and Reggio Emilia · ITScripps Research Institute · USKing's College London · GB

Funding

Brain interleukin-18 control of food intake and energy expenditureR01DK094026 · NIDDK · SCRIPPS RESEARCH INSTITUTE, THE · PI CONTI, BRUNO, ZORRILLA, ERIC P · 2012 to 2013
$745k
Medical Research Council G108/603NIDDK NIH HHS DK094026NIDDK NIH HHS R01 DK094026
6 · The paper itself

Abstract

Interleukin (IL)-18 is a cytokine previously demonstrated to participate in neuroinflammatory processes. Since the components of the IL-18 receptor complex are expressed in neurons throughout the brain, IL-18 is also believed to directly influence neuronal function. Here we tested this hypothesis on mouse hippocampal neurons by measuring the effects of IL-18 on three pathways previously shown to be regulated by this cytokine in non-neuronal cells: the MAPK pathways, p38 and ERK1/2 MAPKs, STAT3 and NF-κB. Experiments were carried out in vitro using the immortalized hippocampal neuronal line HT-22 or in vivo following i.c.v. injection with recombinant mouse IL-18. We showed that IL-18 did not activate NF-κB in HT-22 cells whereas it induced a rapid (within 15min) activation of the MAPK pathways. Moreover, we demonstrated that IL-18 treatment enhanced P-STAT3 (Tyr705)/STAT3 ratio in the nucleus of HT-22 cells after 30-60min of exposure. A similar increase in P-STAT3 (Tyr705)/STAT3 ratio was observed in the whole hippocampus one hour after i.c.v. injection. These data demonstrate that IL-18 can act directly on neuronal cells affecting the STAT3 pathway; therefore, possibly regulating the expression of specific genes within the hippocampus. This effect may help to explain some of the IL-18-induced effects on synaptic plasticity and functionality within the hippocampal system.

Indexed as

AnimalsCells, CulturedExtracellular Signal-Regulated MAP KinasesHippocampusInterleukin-18MaleMiceMice, Inbred C57BLNeuronsNF-kappa Bp38 Mitogen-Activated Protein KinasesReceptors, Interleukin-18Recombinant ProteinsSignal TransductionSTAT3 Transcription FactorExtracellular Signal-Regulated MAP KinasesInterleukin-18NF-kappa Bp38 Mitogen-Activated Protein KinasesReceptors, Interleukin-18Recombinant ProteinsSTAT3 Transcription FactorBrainHippocampusHT-22IL-18IL-18RαIL-18RβIsoformsNF-κBSignalingSTAT-3

Identifiers

PMID24603356
PMCPMC6248908
OpenAlexW2060315442

What OpenQuestion holds

Textmetadata
LicenceTDM
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.