Evidence map›Paper›PMID 25522414›Full record

ArticleThe international journal of neuropsychopharmacology2014

Antidepressant compounds can be both pro- and anti-inflammatory in human hippocampal cells.

Mark Abie Horowitz, Jasmin Wertz, Danhui Zhu, Annamaria Cattaneo, Ksenia Musaelyan, Naghmeh Nikkheslat, Sandrine Thuret, Carmine Maria Pariante, Patricia Ana Zunszain

Open access · bronzeAbstract read
In one paragraph

Article in The international journal of neuropsychopharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
3.5field-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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 79 citations in OpenAlex.

  1. Genetic Contributions of Inflammation to Depression.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2017
    Pooled it
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  4. JZ-1201 modulates depressive-like behaviors in rats through targeting catalase.Naunyn-Schmiedeberg's archives of pharmacology · 2026
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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

9 authors at 1 institution in 1 country.

Mark Abie HorowitzSection of Stress, Psychiatry and Immunology, Department of Psychological Medicine, Institute of Psychiatry, King's College London, London, UK (Dr Horowitz, Ms Wertz, Ms Zhu, Drs Cattaneo, Musaelyan, Nikkheslat, Pariante, and Zunszain); Department of Basic and Clinical Neuroscience, Centre for the Cellular Basis of Behaviour, The James Black Centre (Thuret); and IRCCS Centro San Giovanni di Dio, Fatebenefratelli, Brescia, Italy (Dr Cattaneo).
Jasmin WertzSection of Stress, Psychiatry and Immunology, Department of Psychological Medicine, Institute of Psychiatry, King's College London, London, UK (Dr Horowitz, Ms Wertz, Ms Zhu, Drs Cattaneo, Musaelyan, Nikkheslat, Pariante, and Zunszain); Department of Basic and Clinical Neuroscience, Centre for the Cellular Basis of Behaviour, The James Black Centre (Thuret); and IRCCS Centro San Giovanni di Dio, Fatebenefratelli, Brescia, Italy (Dr Cattaneo).
Danhui ZhuSection of Stress, Psychiatry and Immunology, Department of Psychological Medicine, Institute of Psychiatry, King's College London, London, UK (Dr Horowitz, Ms Wertz, Ms Zhu, Drs Cattaneo, Musaelyan, Nikkheslat, Pariante, and Zunszain); Department of Basic and Clinical Neuroscience, Centre for the Cellular Basis of Behaviour, The James Black Centre (Thuret); and IRCCS Centro San Giovanni di Dio, Fatebenefratelli, Brescia, Italy (Dr Cattaneo).
Annamaria CattaneoSection of Stress, Psychiatry and Immunology, Department of Psychological Medicine, Institute of Psychiatry, King's College London, London, UK (Dr Horowitz, Ms Wertz, Ms Zhu, Drs Cattaneo, Musaelyan, Nikkheslat, Pariante, and Zunszain); Department of Basic and Clinical Neuroscience, Centre for the Cellular Basis of Behaviour, The James Black Centre (Thuret); and IRCCS Centro San Giovanni di Dio, Fatebenefratelli, Brescia, Italy (Dr Cattaneo).
Ksenia MusaelyanSection of Stress, Psychiatry and Immunology, Department of Psychological Medicine, Institute of Psychiatry, King's College London, London, UK (Dr Horowitz, Ms Wertz, Ms Zhu, Drs Cattaneo, Musaelyan, Nikkheslat, Pariante, and Zunszain); Department of Basic and Clinical Neuroscience, Centre for the Cellular Basis of Behaviour, The James Black Centre (Thuret); and IRCCS Centro San Giovanni di Dio, Fatebenefratelli, Brescia, Italy (Dr Cattaneo).
Naghmeh NikkheslatSection of Stress, Psychiatry and Immunology, Department of Psychological Medicine, Institute of Psychiatry, King's College London, London, UK (Dr Horowitz, Ms Wertz, Ms Zhu, Drs Cattaneo, Musaelyan, Nikkheslat, Pariante, and Zunszain); Department of Basic and Clinical Neuroscience, Centre for the Cellular Basis of Behaviour, The James Black Centre (Thuret); and IRCCS Centro San Giovanni di Dio, Fatebenefratelli, Brescia, Italy (Dr Cattaneo).
Sandrine ThuretSection of Stress, Psychiatry and Immunology, Department of Psychological Medicine, Institute of Psychiatry, King's College London, London, UK (Dr Horowitz, Ms Wertz, Ms Zhu, Drs Cattaneo, Musaelyan, Nikkheslat, Pariante, and Zunszain); Department of Basic and Clinical Neuroscience, Centre for the Cellular Basis of Behaviour, The James Black Centre (Thuret); and IRCCS Centro San Giovanni di Dio, Fatebenefratelli, Brescia, Italy (Dr Cattaneo).
Carmine Maria ParianteSection of Stress, Psychiatry and Immunology, Department of Psychological Medicine, Institute of Psychiatry, King's College London, London, UK (Dr Horowitz, Ms Wertz, Ms Zhu, Drs Cattaneo, Musaelyan, Nikkheslat, Pariante, and Zunszain); Department of Basic and Clinical Neuroscience, Centre for the Cellular Basis of Behaviour, The James Black Centre (Thuret); and IRCCS Centro San Giovanni di Dio, Fatebenefratelli, Brescia, Italy (Dr Cattaneo).
Patricia Ana ZunszainSection of Stress, Psychiatry and Immunology, Department of Psychological Medicine, Institute of Psychiatry, King's College London, London, UK (Dr Horowitz, Ms Wertz, Ms Zhu, Drs Cattaneo, Musaelyan, Nikkheslat, Pariante, and Zunszain); Department of Basic and Clinical Neuroscience, Centre for the Cellular Basis of Behaviour, The James Black Centre (Thuret); and IRCCS Centro San Giovanni di Dio, Fatebenefratelli, Brescia, Italy (Dr Cattaneo). patricia.zunszain@kcl.ac.uk.
King's College London · GB

Funding

Medical Research Council G108/603Medical Research Council MR/J002739/1
6 · The paper itself

Abstract

backgroundThe increasingly recognized role of inflammation in the pathogenesis and prognosis of depression has led to a renewed focus on the immunomodulatory properties of compounds with antidepressant action. Studies have, so far, explored such properties in human blood samples and in animal models.

methodsHere we used the more relevant model of human hippocampal progenitor cells exposed to an inflammatory milieu, induced by treatment with IL-1β. This increased the levels of a series of cytokines and chemokines produced by the cells, including a dose- and time-dependent increase of IL-6. We investigated the immunomodulatory properties of four monoaminergic antidepressants (venlafaxine, sertraline, moclobemide, and agomelatine) and two omega-3 polyunsaturated fatty acids (n-3 PUFAs; eicosapentanoic acid [EPA] and docosahexanoic acid [DHA]).

resultsWe found that venlafaxine and EPA were anti-inflammatory: venlafaxine decreased IL-6, with a trend for decreases of IL-8 and IP-10, while EPA decreased the levels of IL-6, IL-15, IL-1RA, and IP-10. These effects were associated with a corresponding decrease in NF-kB activity. Unexpectedly, sertraline and DHA had pro-inflammatory effects, with sertraline increasing IFN-α and IL-6 and DHA increasing IL-15, IL-1RA, IFN-α, and IL-6, though these changes were also associated with a decrease in NF-kB activity, suggesting distinct modes of action. Agomelatine and moclobemide had no effect on IL-6 secretion.

conclusionsThese observations indicate that monoaminergic antidepressants and n-3 PUFAs have distinctive effects on immune processes in human neural cells. Further characterization of these actions may enable more effective personalization of treatment based on the inflammatory status of patients.

Indexed as

Antidepressive AgentsAnti-Inflammatory AgentsCell DifferentiationCells, CulturedCytokinesDose-Response Relationship, DrugEnzyme-Linked Immunosorbent AssayFatty Acids, Omega-3Gene Expression RegulationHippocampusHumansInterleukin-1betaNF-kappa BRNA, MessengerSignal TransductionStem CellsAntidepressive AgentsAnti-Inflammatory AgentsCytokinesFatty Acids, Omega-3Interleukin-1betaNF-kappa BRNA, Messengercytokinesdepressioninflammationneural stem cellsomega-3 fatty acids

Identifiers

PMID25522414
PMCPMC4360247
OpenAlexW2253382469

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LicenceCC BY-NC
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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.