Evidence map›Paper›PMID 30391995›Full record

Trial reportNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2019

Moderators for depressed mood and systemic and transcriptional inflammatory responses: a randomized controlled trial of endotoxin.

Michael R Irwin, Steve Cole, Richard Olmstead, Elizabeth C Breen, Joshua Jin Cho, Mona Moieni, Naomi I Eisenberger

Abstract readRandomized Controlled Trial
PubMed Full text at PMC Publisher
In one paragraph

Trial report in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

31 citing papers in PubMed, 2 syntheses or guidelines pooled it.

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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.

Michael R IrwinCousins Center for Psychoneuroimmunology, Jane and Terry Semel Institute for Neuroscience and Human Behavior, Department of Psychiatry and Biobehavioral Sciences, David Geffen School of Medicine, University of California, Los Angeles, CA, USA. mirwin1@ucla.edu.ORCID http://orcid.org/0000-0002-1502-8431
Steve ColeCousins Center for Psychoneuroimmunology, Jane and Terry Semel Institute for Neuroscience and Human Behavior, Department of Psychiatry and Biobehavioral Sciences, David Geffen School of Medicine, University of California, Los Angeles, CA, USA.
Richard OlmsteadCousins Center for Psychoneuroimmunology, Jane and Terry Semel Institute for Neuroscience and Human Behavior, Department of Psychiatry and Biobehavioral Sciences, David Geffen School of Medicine, University of California, Los Angeles, CA, USA.
Elizabeth C BreenCousins Center for Psychoneuroimmunology, Jane and Terry Semel Institute for Neuroscience and Human Behavior, Department of Psychiatry and Biobehavioral Sciences, David Geffen School of Medicine, University of California, Los Angeles, CA, USA.
Joshua Jin ChoCousins Center for Psychoneuroimmunology, Jane and Terry Semel Institute for Neuroscience and Human Behavior, Department of Psychiatry and Biobehavioral Sciences, David Geffen School of Medicine, University of California, Los Angeles, CA, USA.ORCID http://orcid.org/0000-0002-8629-8500
Mona MoieniCousins Center for Psychoneuroimmunology, Jane and Terry Semel Institute for Neuroscience and Human Behavior, Department of Psychiatry and Biobehavioral Sciences, David Geffen School of Medicine, University of California, Los Angeles, CA, USA.
Naomi I EisenbergerDepartment of Psychology, University of California, Los Angeles, CA, USA.

Funding

Inflammation-Induced Depressed Mood: The Role of Social Neurocognitive MechanismsR01MH091352 · NIMH · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI EISENBERGER, NAOMI ILANA · 2010 to 2013
$1.7M
Sleep loss as a vulnerability factor for inflammation induced depressive symptoms in older womenK23AG049085 · NIA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI CHO, JOSHUA HYONG-JIN · 2015 to 2019
$950k
NIA NIH HHS K23 AG049085U.S. Department of Health & Human Services | NIH | National Institute of Mental Health (NIMH) R01MH091352
6 · The paper itself

Abstract

Activation of the innate immune system is thought to contribute to depression. Multiple social and behavioral factors are also known to instigate depression. Whether these socio-behavioral factors interact with inflammatory stimuli to alter proinflammatory responses and depressed mood is not known. In 115 healthy adults, social, emotional, and behavioral factors were assessed at baseline. A single infusion of endotoxin (Escherichia coli; 0.8 ng/kg of body weight) or placebo (0.9% saline) was administered with hourly assessment of depressed mood and proinflammatory cytokines (interleukin-6 (IL-6); tumor necrosis factor-α (TNF)). Inflammatory gene expression was examined at 30 min after infusion, prior to increase of inflammatory cytokines. As compared to placebo, endotoxin-induced increases of depressed mood were moderated by baseline levels of perceived stress, trait sensitivity to social disconnection, and severity of symptoms of anxiety and depression (all Ps < 0.05) but not early life stress, social status, social support, neuroticism, or sleep disturbance. Anxiety symptoms remained significant in multivariable analyses (P < 0.01). None of these socio-behavioral factors were related to increases in proinflammatory cytokines. Transcriptome profiling analyses indicated that perceived stress, sensitivity to social disconnection, and depressive symptoms were associated with increased activation of pro-inflammatory transcription control pathways (i.e., activator protein-1, nuclear factor-κB) in response to endotoxin (all Ps < 0.05). These results indicate that an array of socio-behavioral factors, which are associated with depression risk, modify vulnerability to inflammation-induced depressed mood. Together, these observations may be used to help target therapeutic interventions to mitigate occurrence of the inflammatory biotype of depression.

Indexed as

AnxietyDepressionInflammationStress, PsychologicalAdultAdverse Childhood ExperiencesDouble-Blind MethodEndotoxinsFemaleGene ExpressionGene Expression ProfilingHumansInterleukin-6MaleNeuroticismNF-kappa BEndotoxinsIL6 protein, humanInterleukin-6NF-kappa BTNF protein, humanTranscription Factor AP-1Tumor Necrosis Factor-alpha

Identifiers

PMID30391995
PMCPMC6333799

What OpenQuestion holds

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Registered trials

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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.